Fluid and Electrolytic ImbalancePrepared by: Tesfa D. (ANP)-2010First Edition-2014*

ObjectivesAt the end of this chapter, the learner be able to:Discuss the anatomy and physiology of body fluids and electrolytesDescribe common fluid and electrolyte changes, their causes and managementIdentify common acid base imbalances and their treatment*

Fluid volume imbalanceHyper osmolar imbalanceHypo osmolar imbalanceIsotonic volume deficitIsotonic volume excess*

Fluid volume deficit (hypovolemia)Loss of ECF > intake of fluidElectrolytes to water ratio is the sameHypovolemia Vs Dehydration*

ContdCausesInadequate intakeAbn. fluid lossesThird-space fluid shiftsRisk factors Diabetes insipidusAdrenal insufOsmotic diuresisHemorrhageComa

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ContdClinical ManifestationsSkin-cool, clammy, decreased skin turgorCVS-postural hypotension; a weak, rapid heart rate; flattened neck veins; GUS-oliguria; concentrated urine.Mouth-dry mucus membrane.Others-acute weight loss; thirst; anorexia; nausea; lassitude; muscle weakness; and cramps.*

ContdAssessment and diagnostic findingsHxPEBUNHCTUrine specific gravity Urine osmolalitySerum electrolyte*

ContdMedical ManagementMild to moderate (5-10%);Oral fluid intake-small frequent sipFrequent mouth careGiving non-irritating fluid Acute and severe (>15%);IV route is required (1L/30min-1hr)Isotonic electrolyte solutions *

ContdNursing ManagementMonitoring;Fluid intake and output. Daily body weight.Vital signs closely.Skin and tongue turgor.*

Fluid volume excess (hypervolemia)An isotonic expansion of the ECF Water to sodium proportion is the same*

ContdCauseIatrogenicHeart failureRenal failureCirrhosis of the liverExcessive sodium salts intakeExcessive administration of sodium*

ContdClinical ManifestationsEdema Distended neck veinsCrackles, tachycardia; increased BP, PP, and CVPIncreased weight, urine outputShortness of breathWheezing.*

ContdAssessment and Diagnostic FindingsBUN.Hematocrit.Serum osmolality.Chest x-rays.*

ContdMedical ManagementFluid restrictionPharmacologic: diureticsHemodialysis/peritoneal dialysisNutritional

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ContdNursing ManagementMeasures intake and outputAssess breath soundsMonitors the degree of edemaMaintaining semi-fowlers positionFrequent positioningTeaching patient about edema *

Electrolyte Imbalance Sodium;Primary determinant of ECF osmolality.Most abundant electrolyte in ECF. Controls water distribution.Muscle contraction and transmission of nerve impulses.135 to 145 mEq/L (135145 mmol/L).One millimol/kg, excreted by kidney.Sodium deficit and excess.*

Sodium deficit (hyponatremia)Less than 135 mEq/L [135 mmol/L]).Occurs when;Low quantity of total body sodiumNormal total body sodium contentAn excess of total body sodium

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ContdCausesSodium loss Diuretics use Low-salt diet Adrenal insufficiencyWater intoxication

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ContdPredisposing factors SIADHHyperglycemiaElectrolyte-poor parenteral fluidsUse of tap-water enemasExcessive parenteral administration of dextrose and water solutionsCompulsive water drinking*

ContdClinical ManifestationsPoor skin turgorDry mucosaDecreased saliva productionOrthostatic fall in blood pressure, Nausea Abdominal crampingAltered mental status*

ContdWhen the serum sodium level drops below 115 mEq/L (115 mmol/L);lethargyConfusion signs of muscle twitching increasing focal weakness intracranialHemiparesis pressurepapilledemaSeizures

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ContdAssessment and Diagnostic FindingsSerum sodium level Serum osmolality Urinary sodium content Urine specific gravity*

ContdMedical ManagementSodium replacement-12 mEq/L in 24 hrsDiuretic-furosemide (Lasix)Water restriction-800 mL in 24 hrs*

ContdNursing ManagementIdentification of patients at risk and early detection and treatmentMonitor fluid intake/output and daily body weightsNote abnormal losses of sodium or gains of water and GI manifestationsAlert for central nervous system changes*

Sodium excess (hypernatremia)Exceeding 145 mEq/L [145 mmol/L].Occurs when;Gain of sodium in excess of water Loss of water in excess of sodium*

ContdCausesFluid deprivationHigh sodium intakeIV administration of hypertonic saline or excessive use of sodium bicarbonateWater loss Diabetes insipidusHeat stroke, near-drowning, e.t.c*

ContdClinical ManifestationsModerate:-restlessness and weaknessSevere:- disorientation, delusions, and hallucinationsOthers:-Dry swollen tongue, Sticky mucous membranes, Flushed skin, Peripheral and pulmonary edema, Postural hypotension, e.t.c*

ContdAssessment and Diagnostic FindingsSerum sodium level Serum osmolality Urine specific gravity Urine osmolality

What do you expect if the cause is DI?*

ContdMedical ManagementIV hypotonic electrolyte solution0.3% sodium chloride-saferDextrose 5% in water [D5W]) DiureticsDesmopressin acetate (DDAVP) *

ContdNursing ManagementFluid losses and gains are carefully monitoredAssess for abnormal losses of water or low water intake and for large gains of sodium.Obtain a medication history.Monitors for changes in behavior.*

ContdPreventionAdequate fluid intakeDebilitated patients at regular intervals.Alternate route for intake.Diabetes insipidus.*

Potassium imbalance98% is inside the cells, in SKM3.5 to 5.5 mEq/L (3.55.5 mmol/L).Daily requirement is 1mmol/kg.Neuromuscular function Sodium-potassium pump*

Potassium deficit (hypokalemia)Less than 3.5mEq/L (3.5 mmol/L).Hypokalemia may occur in patients with;Normal potassium storesAlkalosis Hypokalemia is a common imbalance.*

ContdCauses GI loss of potassium (most common)Recent ileostomyVillous adenomaAlkalosisHyperaldosteronismHigh-carbohydrate parenteral fluidsMagnesium depletion*

ContdClinical ManifestationsSevere-death Dysrhythmias, Muscle weakness Leg cramps, Fatigue, VAN Decreased bowel motility Glucose intolerance Paresthesias Increased sensitivity to digitalis*

ContdAssessment and diagnostic findingsECGFlat T waves and/or inverted T wavesDepressed ST segments An elevated U waveUrinary potassium*

ContdMedical ManagementPotassium replacement (IV/Oral)40 to 80 mEq/day-no risk of potassium loss50 to 100 mEq/day-risky potassium loss*

ContdNursing ManagementMonitor for its early presence in patients at risk Monitoring of fluid intake and output Monitor closely for signs of digitalis toxicity*

ContdPreventing hypokalemiaEncouraging the patient at risk to eat foods rich in potassium, such as fruit and fruit juices (bananas, citrus fruit), fresh and frozen vegetables, fresh meats, and processed foods. (when the diet allows).*

Potassium excess (hyperkalemia)Greater than 5.5 mEq/L (5.5 mmol/L).Pseudohyperkalemia-falsely high level of potassium;Use of a tight tourniquet around an exercising extremity Hemolysis of the sample before analysis. Marked leukocytosis Drawing blood above a site where potassium is infusing

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ContdCauses Infection.Decreased renal excretion of potassium. Excessive intake of potassium in foodHypoaldosteronism. Addisons disease.Acidosis. Medications (in more than 60% )*

ContdClinical ManifestationsDisturbances in cardiac conductionVentricular dysrhythmias and cardiac arrest Skeletal muscle weakness and even paralysisGI manifestations*

ContdAssessment and Diagnostic FindingsSerum potassium levels.ECG changes. Arterial blood gas analysis (metabolic acidosis).*

ContdMedical ManagementRestriction of potassium source. Cation exchange resins (eg, Kayexalate).10-20 units of reg.insulin and 25-50g of glucose. 10 ml of 10% calcium gluconate. Dialysis.Avoid exogenous potassium.*

ContdEmergency pharmacologic therapyIV calcium gluconate, sodium, regular insulin and a hypertonic dextrose solution.Monitoring the blood pressure. Extra caution is required if the patient has been digitalized.Beta-2 agonistsECG monitoring during administration*

ContdNursing ManagementMonitor closely for signs of hyperkalemia.Avoid prolonged use of tourniquet and exercise.Blood sample should be delivered to the laboratory as soon as possible.

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Calcium imbalanceCalcium >99% in the skeletal systemAbout 1% is rapidly exchangeable Bounded, ionized, complexed8.5 to 10.5 mg/dL (2.12.6 mmol/L)Absorbed from foods Excreted in the fecesControlled by PTH and calcitonin

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ContdFunction;Transmitting nerve impulses Regulate muscle contraction and relaxationActivating enzymes Blood coagulation

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Calcium deficit (hypocalcemia)Less than 8.5 mg/dLCausesPrimary hypoparathyroidism Surgical hypoparathyroidism (more common). Massive dministration of citrated blood (transient hypocalcemia).PancreatitisRenal failure*

ContdClinical ManifestationsTetany (most) Spasms of muscles of the extremities and facePain, seizure, hyperactive tendon reflexes+Ve Chvosteks and Trousseaus sign-lateECG and mental status changes *

ContdAssessment and Diagnostic FindingsSerum calciumABGASerum albumin*

ContdMedical ManagementCalcium rich food (1,000 to 1,500 mg/day)Parenteral calcium saltsVitamin D therapyAluminum hydroxide, calcium acetate, or calcium carbonate antacids.*

ContdNursing ManagementObserve for hypocalcemia in patients at risk.Seizure precautions.Health education.*

Calcium excess (hypercalcemia)Greater than 8.5 mg/dL, >16 mg/dLHypercalcemic crisis- >17 mg/dL, 50% mortality rateCauses Malignancies and hyperparathyroidism (most common). Immobility.Thiazide diuretics.Milk-alkali syndrome.Vitamin A and D intoxication. Lithium use.*

ContdClinical ManifestationsMuscle weaknessCNS presentationVAN ConstipationCardiac standstillDigitalis toxicityDehydrationAbdominal and bone pain *

ContdAssessment and Diagnostic FindingsThe serum calcium level ECG changesPTH testX-rays The Sulkowitch urine test*

ContdMedical ManagementGeneral measuresAdministering fluids to dilute serum calcium and promote its excretion by the kidneys.Mobilizing the patient.Restricting dietary calcium intake.*

ContdPharmacologic therapy0.9% sodium chloride solution.Administering IV phosphate.Furosemide (Lasix)MithramycinBisphosphonates Inorganic phosphate saltsCalcitonin (salmon)Corticosteroids*

ContdNursing ManagementMonitor the patients at risk. Encourage hospitalized patient to move.Encouraged fluid intake. Adequate fiber diet.Assess for signs and symptoms of digitalis toxicity. Cardiac rate and rhythm are monitored.*

Reading Assignment Read about;Magnesium ImbalancesPhosphorus ImbalancesChloride Imbalances *

Acid-Base BalanceAcid; Higher concentration of hydrogen ionsBase;Higher concentration of hydroxide ions*

ContdpH;Alkalinity or acidity of a substance.Potential of hydrogen.Measured on a scale 0-14.Hydrogen ion concentration.Normal Blood pH is 7.35 7.45.pH decreases-acidity increases.pH increases-acidity decreases.

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Regulation of Acid - Base BalanceBuffer systems: bicarbonate and carbonic acid, phosphates, serum proteins and meth-hemoglobinRespiratory system.Renal system.*

ContdCarbonic Acid-Bicarbonate Buffer SystemPrimary extracellular fluid buffer system.Maintains a ratio of 20 parts bicarbonate to 1 part carbonic acid.Uses the process of hydration of CO2 to break it down so it can be neutralized.*

ContdRespiratory RegulationRespiratory System regulates by adjusting rate and depth of respirations.By increasing rate and depth more CO2 will be blown off.By decreasing rate and depth CO2 will be conserved.*

ContdRenal RegulationWorks slower than respiratory compensation.Effects are more long lasting.Primarily regulates amount of bicarbonate absorbed or excreted.Also regulates ammonia and electrolytes which can effect acid-base.*

Acid-base Imbalance AlkalosisRespiratoryMetabolicAcidosisRespiratoryMetabolic*

Respiratory AlkalosisDeficiency of carbon dioxide.PCO2 below 31 mmHg.Too much carbon dioxide is released.Causes:HyperventilationHypoxemiaHigh altitudesSalicylate overdose*

ContdClinical ManifestationsNumbness/tingling in extremitiesLightheadednessConfusion/ agitation, vent. fibrillationHeart palpitations, ventr. arrhythmias Muscle crampingDeep rapid respirationspH high (>7.45)pCO2 low (

ContdManagement Treat causeOxygenRe-breathing CO2Compensation kidneys will attempt to compensate by excreting more bicarbonate*

ContdNursing Care Relieve anxietySedationReassurancePaper bagRest*

Respiratory AcidosisExcess acid (CO2)Causes:HypoventilationAnesthesiaSedativesCOPDRespiratory infectionsInadequate ventilatory managementExcessive CO2 production*

ContdClinical ManifestationsDecreased rate and depth of respirationsHypoxiaHypotensionHypercapnic encephalopathypH low (< 7.35)PCO2 high (>45mmHg)*

ContdManagement Treat causeVentilatory supportPulmonary hygieneEmotional support*

Metabolic AlkalosisExcess of baseCausesGain of baseLoss of too much acidHypokalemia*

ContdClinical Manifestations Shallow breathing, Cheyne-stokes respNausea/vomiting/diarrheaConfusionNumbness / tinglingHypocalcemiaHypokalemiapH high (> 7.45)HCO3 high (>26)*

ContdManagementReplace fluids and electrolytes.Diamox (Acetazolamide) enhances excretion of bicarbonate.Proper functioning kidneys will excrete excess bicarbonate with adequate fluid volume and appropriate potassium.*

ContdNursing Care Monitor vital signs closely.Monitor fluid status.Safety measures ( change in level of consciousness).If nasogastric suction, irrigate with NS, not water.

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Metabolic AcidosisAcid excess or base deficitCausesRenal failureDiabetic ketoacidosisLactic acidosisLarge amount drainage from ileostomy tubeMalnutritionAnaerobic tissue metabolism*

ContdClinical Manifestations Nausea/ vomiting/ diarrheaKussmauls respirationsFruity-smelling breatheHyperkalemiaBradycardiapH low (< 7.35)HCO3 low (< 22)*

ContdManagementTreat causeAdminister bicarbonate in extreme casesReplace fluids and electrolytesSafety*

The End!*

*Various types of FVI could occur.The variation is the result of which component the fluid is excess or deficient.Types of FVI;Hyper osmolar imbalance:- water in ECF is less than the solute proportion normally expected.Hypo osmolar imbalance:- water in ECF is excess.Isotonic volume deficit:- whole deficit in ECF (electrolyte and water).Isotonic volume excess:- whole excess.

*Occurs when loss of extracellular fluid (water and electrolytes) volume in the same proportion exceeds the intake of fluid. The ratio of serum electrolytes to water remains the same.Dehydration-to loss of water alone with serum electrolyte level is the same.Fluid volume deficit (hypovolemia) should notbe confused with the term dehydration,*Causesinadequate intakeNausea and inability to gain access to fluidsabnormal fluid losses; vomiting, diarrhea, GI suctioning, sweating, third-space fluid shiftsRisk factors diabetes insipidusadrenal insufficiencyosmotic diuresishemorrhagecoma

, or the movement of fluid from the vascular system toother body spaces (eg, with edema formation in burns or asciteswith liver dysfunction), also produce FVD.

*Clinical Manifestationscan be mild, moderate, or severeSkin-cool, clammy, decreased skin turgor. CVS-postural hypotension; a weak, rapid heart rate; flattened neck veins; increased temperature; decreased central venous pressure.GUS-oliguria; concentrated urine.Mouth-dry mucus membrane.Others-acute weight loss; thirst; anorexia; nausea; lassitude; muscle weakness; and cramps.

*Assessment and diagnostic findingsBUN elevated out of proportion to the serum creatinine level (a ratio greater than 20:1).hematocrit level is increased.Urine specific gravity is increased.Urine osmolality is greater than 450 mOsm/Kg.Hyperkalemia.Decreased central venous pressure with normal cardiovascular function.

Gerontologic ConsiderationsElderly patients have special nursing care needs because of theirpropensity for developing fluid and electrolyte imbalances (Beck,2000; Kugler & Hustead, 2000). Fluid balance in the elderlypatient is often marginal at best because of certain physiologicchanges associated with the aging process. Some of these changesinclude reduction in total body water (associated with increasedbody fat content and decreased muscle mass); reduction in renalfunction, resulting in decreased ability to concentrate urine; decreasedcardiovascular and respiratory function; and disturbancesin hormonal regulatory functions. Although these changes areviewed as normal in the aging process, they must be consideredwhen the elderly person becomes ill because age-related changespredispose the person to fluid and electrolyte imbalances. Thesephysiologic changes must be considered during assessment of theelderly patient as well as before initiating treatment for fluid andelectrolyte imbalances.Assessment of the elderly patient should be modified somewhatfrom that of younger adults. For example, skin turgor is lessvalid in the assessment of elderly patients because their skin haslost some of its elasticity; therefore, other assessment measures(eg, slowness in filling of veins of the hands and feet) becomemore important in detecting FVD. In the elderly patient, skinturgor is best tested over the forehead or the sternum, because alterationsin skin elasticity are less marked in these areas. As in anypatient, skin turgor should be monitored serially to detect subtlechanges.The nurse should perform a functional assessment of the agedpersons ability to determine fluid and food needs and to obtainadequate intake. For example, is the patient mentally clear? Is thepatient able to ambulate and use both arms and hands to reachfluids and foods? Is the patient able to swallow? All of these questionshave a direct bearing on how patients will be able to meettheir own need for fluids and foods. During an elderly patientshospital stay, the nurse must provide fluids for any patient whois unable to carry out self-care activities.Another concern is that some elderly patients deliberately restricttheir fluid intake to avoid embarrassing episodes of incontinence.In this situation, the nurse also identifies interventionsto deal with the incontinence, such as encouraging the patient towear protective clothing or devices, carry a urinal in the car, orpace fluid intake to allow access to toilet facilities during the day.Elderly people without cardiovascular or renal dysfunction shouldbe reminded to drink adequate fluids.*Medical ManagementMild to moderate;Oral fluid intake-small frequent sip.Frequent mouth care.Giving non irritating fluid. Acute and severe;IV route is required. Isotonic electrolyte solutions (e.g, lactated Ringers or 0.9% sodium chloride).As soon as the patient becomes normotensive, a hypotonic electrolyte solution (eg, 0.45% sodium chloride). Accurate and frequent assessments of intake and output, weight, vital signs, central venous pressure, level of consciousness, breath sounds, and skin color should be performed not to avoid overload the patient.

The Rate depends on the degree of dehydration. It should be fast until the vital signsare corrected and adequate urine output is achieved. One liter over 30 minutes to onehour can be given for severe dehydration.

*Nursing ManagementMonitors and measures fluid intake and output at least every 8 hours, and sometimes hourly.Monitoring daily body weights.Wt loss of 0.5 kg 500 mL fluid loss.Monitoring vital signs closely.Skin and tongue turgor is monitored on a regular basis.

The nurse observes for aweak, rapid pulse and postural hypotension (ie, a drop in systolicpressure exceeding 15 mm Hg when the patient moves from alying to a sitting position). A decrease in body temperature oftenaccompanies FVD, unless there is a concurrent infection.

PreventionIdentify patients at risk.Takes measures to minimize fluid losses. For example, if the patient has diarrhea, diarrhea use antidiarrheal medications and small volumes of oral fluids at frequent intervals.

*an isotonic expansion of the ECF caused by the abnormal retention of water and sodium in approximately the same proportions in which they normally exist in the ECF. is always secondary to an increase in the total body sodium content, which, in turn, leads to an increase in total body water. related to simple fluid overload or diminished function of the homeostatic mechanisms responsible for regulating fluid balance.

*Contributing factors can include heart failure, renalfailure, and cirrhosis of the liver. Another contributing factor isconsumption of excessive amounts of table or other sodium salts.Excessive administration of sodium-containing fluids in a patientwith impaired regulatory mechanisms may predispose him or herto a serious FVE as well (Beck, 2000).*Clinical Manifestationsedemadistended neck veinscrackles (abnormal lung sounds)tachycardia; increasedblood pressure, pulse pressure, and central venous pressureincreased weight increased urine outputshortness of breathwheezing.functional murmurs

*Assessment and Diagnostic FindingsBUN and hematocrit levels decreased.Serum osmolality decreased.Chest x-rays may reveal pulmonary congestion.

*Medical ManagementDirected at the causes.Pharmacologic;Diuretics are prescribed when dietary restriction of sodium alone is insufficient to reduce edema.The choice of diuretic is based onseverity of the hypervolemic state. the degree of impairment of renal function.potency of the diuretic.Thiazide diuretics;5% to 10% of filtered sodium excreted.Act on distal tubule.Ordered for mild to moderate hypervolemia.Loop diuretics;Act on loop of henle.20% to 30% of filtered sodium is excreted.Ordered for severe hypervolemia.Hemodialysis/peritoneal dialysis; A choice when renal function is severely impaired that diuretics cannot act efficiently.Used to remove;nitrogenous wastes control potassiumacidbase balance to remove sodium and fluid. Hemodialysis/peritoneal dialysis; A choice when renal function is severely impaired that diuretics cannot act efficiently.Used to remove;nitrogenous wastes control potassiumacidbase balance to remove sodium and fluid. Nutritional;An average daily diet not restricted in sodium contains 6 to 15 g of salt.The restriction vary from mild to 250 mg of sodium per day.It is the sodium salt, sodium chloride, rather than sodium itself that contributes to edema.

*Nursing ManagementMeasures intake and output.Assess breath sounds.Monitors the degree of edema in the most dependent parts of the body, such as the feet and ankles in ambulatory patients and the sacral region in bedridden patients.Maintaining semi fowlers position.Frequent positioning.Teaching patient about edema.

The degree of pitting edema is assessed, and the extent ofperipheral edema is monitored by measuring the circumferenceof the extremity with a tape marked in millimeters.*Sodium Imbalancesodium is the primary determinant of ECF osmolality.Most abundant electrolyte in ECF. Controls water distribution throughout the body.The primary regulator of ECF volume as its movement coupled with water.Necessary for muscle contraction and the transmission of nerve impulses.Its normal concentration ranges from 135 to 145 mEq/L (135145 mmol/L).

Sodium proportion change in plasma may be due to;Low sodium amount with low water where the magnitude of sodium loss is greater in proportion.Normal sodium amount with greater amount of total body water.Sodium is greater with an even greater body water gain. Sodium is greater with normal body water or decreased total body water.

Sodium deficit and excess are the two most common sodium imbalances.

The fact that sodium does not easily cross the cell wallmembrane, plus its abundance or high concentration, accountsfor its primary role in controlling water distribution throughoutthe body.*Serum sodium level that is below normal (less than 135 mEq/L [135 mmol/L]).Can be superimposed on an existing FVD or FVE.Occurs when;low quantity of total body sodium with a lesser reduction in total body water,normal total body sodium content with excess total body water,an excess of total body sodium with an even greater excess of total body water.

Plasma sodium concentrationrepresents the ratio of total body sodium to total bodywater. A decrease in this ratio can occur from a low quantity oftotal body sodium with a lesser reduction in total body water,normal total body sodium content with excess total body water,and an excess of total body sodium with an even greater excess oftotal body water. However, a hyponatremic state can be superimposedon an existing FVD or FVE.*CausesSodium loss due to vomiting, diarrhea, fistulas, or sweating.Diuretics use. a low-salt diet. Adrenal insufficiencyWater intoxication (dilutional hyponatremia);No loss of sodium but excess amount of water in ECF (hyper osmolar state is created).*Predisposing factors are; SIADH.Hyperglycemia.electrolyte-poor parenteral fluids.use of tap-water enemas, or the irrigation of nasogastric tubes with water instead of normal saline solution.excessive parenteral administration of dextrose and water solutions.compulsive water drinking (psychogenic polydipsia).

*Clinical Manifestationsdepend on the cause, magnitude, and speed with which the deficit occurs.Poor skin turgordry mucosadecreased saliva production, orthostatic fall in blood pressure, nausea abdominal crampingaltered mental statusanorexia, muscle cramps, and a feeling of exhaustion if it is associated with sodium loss and water gain

*In general, patients with an acute decrease in serumsodium levels have more severe symptoms and higher mortalityrates than do those with more slowly developing hyponatremia.*Assessment and Diagnostic FindingsSerum sodium level is less than 135 mEq/L (regardless of th cause).Serum sodium level 100 mEq/L (100 mmol/L) or less (SIADH).Serum osmolality is also decreased.Urinary sodium content is less than 20 mEq/L (20 mmol/L) (Sodium loss).Urinary sodium content is greater than 20 mEq/L (SIADH). Urine specific gravity is 1.002 to 1.004 (Sodium loss). Urine specific gravity over 1.012 (SIADH).

Although the patient with SIADH retainswater abnormally and thus gains body weight, there is no peripheraledema; instead, fluid accumulates inside the cells. Thisphenomenon is sometimes manifested as fingerprinting whenthe finger is pressed over a bony prominence, such as the sternum.*Medical ManagementSodium replacement:-sodium lossFor patients who can eat and drink, sodium is easily replaced by mouth.For those who cannot consume sodium, lactated Ringers solution or isotonic saline (0.9% sodium chloride) solution may be prescribed parenteraly.The maximum serum sodium replacement is 12 mEq/L in 24 hours, to avoid neurologic damage due to osmotic demyelination.Rapidly replacement above 140 mEq/L produce lesions in the pons that cause paraparesis, dysarthria, dysphagia, and coma.SIADHAdministration of hypertonic saline solution alone cannot change the plasma sodium concentration. Diuretic furosemide (Lasix).Water restrictionIn a patient with normal or excess fluid volume.restricting fluid to a total of 800 mL in 24 hours.

The key to treating hyponatremia is assessment; this includes thespeed with which hyponatremia occurred rather than relying onlyon the patients actual serum sodium value (Fall, 2000).

In SIADH, the administration of hypertonic saline solutionalone cannot change the plasma sodium concentration. Excesssodium would be excreted rapidly in a highly concentrated urine.With the addition of the diuretic furosemide (Lasix), urine is notconcentrated and isotonic urine is excreted to effect a change inwater balance. In patients with SIADH, in whom water restrictionis difficult, lithium or demeclocycline can antagonize the osmoticeffect of ADH on the medullary collecting tubule.When neurologic symptoms are present, however, it may be necessaryto administer small volumes of a hypertonic sodium solution,such as 3% or 5% sodium chloride. Incorrect use of thesefluids is extremely dangerous because 1 L of 3% sodium chloridesolution contains 513 mEq of sodium, and 1 L of 5% sodiumchloride solution contains 855 mEq of sodium. If edema existsalone, sodium is restricted; if edema and hyponatremia occurtogether, both sodium and water are restricted.

*Nursing ManagementIdentification of patients at risk and early detection and treatment of to avoid complication.Monitor fluid intake and output as well as daily body weights.Note abnormal losses of sodium or gains of water and GI manifestations, such as anorexia, nausea, vomiting, and abdominal cramping.Alert for central nervous system changes, such as lethargy, confusion, muscle twitching, and seizures.

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With a water loss, the patient loses more water than sodium; as a result, the serum sodium concentration increases and the increased concentration pulls fluid out of the cell. This is both an extracellular and intracellular FVD. In sodium excess, the patient ingests or retains more sodium than water.*CausesFluid deprivation in unconscious patients. Administration of hypertonic enteral feedings. IV administration of hypertonic saline or excessive use of sodium bicarbonateWatery diarrhea and greatly increased insensible water loss (e.g, hyperventilation, denuding effects of burns).Diabetes insipidus.

Less common causes are;heat strokenear-drowning in sea water (which contains a sodium concentration of approximately 500 mEq/L), malfunction of either hemodialysis or peritoneal dialysis proportioning systems. *Clinical ManifestationsPrimarily neurologic and are presumably the consequence of cellular dehydration.Moderate:-restlessness and weaknessSevere:- disorientation, delusions, and hallucinationsOther signs; Dry swollen tongue Sticky mucous membranes.Flushed skinPeripheral and pulmonary edemaPostural hypotensionIncreased muscle tone and deep tendon reflexes Mild rise in body temperature

Dehydration (resulting in hypernatremia) is often overlooked asthe primary reason for behavioral changes in the elderly patient.If hypernatremia is severe, permanent brain damage can occur(especially in children). Brain damage is apparently due to subarachnoidhemorrhages that result from brain contraction.A primary characteristic of hypernatremia is thirst. Thirst is sostrong a defender of serum sodium levels in healthy people thathypernatremia never occurs unless the person is unconscious oris denied access to water. Unfortunately, ill people may have animpaired thirst mechanism. *Assessment and Diagnostic FindingsSerum sodium level exceeds 145 mEq/L (145 mmol/L).Serum osmolality exceeds 295 mOsm/kg (295 mmol/L). The urine specific gravity and urine osmolality are increased. What do you expect if the cause is DI?

*Medical ManagementInfusion of a hypotonic electrolyte solution (e.g, 0.3% sodium chloride) or an isotonic nonsaline solution(eg, dextrose 5% in water [D5W]). D5W is indicated when water needs to be replaced without sodium. Hypotonic sodium solution to be safer than D5W because it allows a gradual reduction in the serum sodium level and decreases the risk of cerebral edema. Hypotonic sodium solution is the solution of choice in severe hyperglycemia with hypernatremia.Diuretics also may be prescribed to treat the sodium gain.Desmopressin acetate (DDAVP) may be prescribed to treat diabetes insipidus if it is the cause of hypernatremia. How it can act ?N.B. The serum sodium level is reduced at a rate no faster than 0.5 to 1 mEq/L to allow sufficient time for readjustment through diffusionm across fluid compartments.

*Nursing Managementfluid losses and gains are carefully monitoredAssess for abnormal losses of water or low water intake and for large gains of sodium.Obtain a medication history because some prescription medications have a high sodium content.Note the patients thirst or elevated body temperature and evaluates it in relation to other clinical signs. The nurse monitors for changes in behavior, such as restlessness, disorientation, and lethargy.

*98% of the bodys potassium is inside the cells (major intracellular electrolyte).Normal serum potassium concentration ranges from 3.5 to 5.5 mEq/L (3.55.5 mmol/L).Important in neuromuscular function (that is 2% is in the ECF).Under the influence of the sodium-potassium pump and based on the bodys needs, potassium is constantly moving in and out of cells.

*Serum potassium concentration level is less than 3.5mEq/L (3.5 mmol/L).Hypokalemia may occur in patients with normal potassium stores; however, when alkalosis is present, a temporary shift of serum potassium into the cells occurs. Hypokalemia is a common imbalance .

*Causes GI loss of potassium (most common).VomitingDiarrhea Prolonged gastric suctionLaxative Recent ileostomyVillous adenomaAlkalosis HyperaldosteronismHigh-carbohydrate parenteral fluids.Magnesium depletionExcessive renal excretion e.g. Diuretic useMedication Potassium-losing diuretics, such as thiazides (eg, chlorothiazide)Corticosteroids Penicillins (e.g. sodium penicillin, Carbenicillin)Amphotericin BPoor potassium diet intake;Debilitated elderly peopleAlcoholics Anorexia nervosaBulimia.

Intestinal fluid may contain as much potassium as 30 mEq/L. Villous adenoma (a tumor of the intestinal tract characterized by excretion of potassium rich mucus).For example, hydrogen ions move out of the cells in alkalotic states to help correct the high pH, and potassium ionsmove in to maintain an electrically neutral state. (This is discussedfurther in the section on acidbase balance.)

*Clinical ManifestationsSevere-death through cardiac or respiratory arrest. Dysrhythmias Anorexia Nausea Vomiting Muscle weakness Leg cramps Decreased bowel motility Fatigue Glucose intolerance Paresthesias Increased sensitivity to digitalisIf prolongedPolyuriaNocturia Excessive thirst

*Assessment and diagnostic findingsECGFlat T waves and/or inverted T wavesDepressed ST segments An elevated U waveIncreased sensitivity to digitalis Urinary potassium excretion exceeding 20 mEq/24 h with hypokalemia suggests that renal potassium loss is the cause.

*Medical ManagementAdministration of 40 to 80 mEq/day of potassium in adult , if no abnormal loss of potassium .Dietary intake of potassium in the average adult is 50 to 100 mEq/day, if risky for potassium loss. Foods high in potassium;Fruits (especially raisins, bananas, apricots, and oranges)Vegetables, legumes, whole grains, milk, and meat.Oral potassium supplements (salt substitutes contain 50 to 60 mEq of potassium per teaspoon).When oral administration of potassium is not feasible, the IV route is indicated.The IV route is mandatory for patients with severe hypokalemia (e.g., a serum level of 2 mEq/L). E.g. potassium chloride, potassium acetate or potassium phosphate.For routine maintenance needs, potassium is suitably diluted and administered at a rate no faster than 10 mEq/h. Even in extreme hypokalemia, however, potassium should be administered no faster than 20 to 40 mEq/h (suitably diluted). In critical situations, more concentrated solutions (such as 40 mEq/L) may be administered through a central line.

*Nursing ManagementMonitor for its early presence in patients at risk. Monitoring of fluid intake and output is necessary because 40 mEq of potassium is lost for every liter of urine output.When available, the ECG may provide useful information.Patients receiving digitalis who are at risk for potassium deficiency should be monitored closely for signs of digitalis toxicity. Physicians usually prefer to keep the serum potassium level above 3.5 mEq/L (3.5 mmol/L) in patients receiving digitalis medications such as digoxin.

**Serum potassium concentration greater than 5.5 mEq/L (5.5 mmol/L).Pseudohyperkalemia Falsely high level of potassium Causes;Use of a tight tourniquet around an exercising extremity Hemolysis of the sample before analysis. Marked leukocytosis (white blood cell count exceeding 200,000) or thrombocytosis (platelet count exceeding 1 million),Drawing blood above a site where potassium is infusing.

*Causes Decreased renal excretion of potassium. Infection.Excessive intake of potassium in food or medications. Hypoaldosteronism. Addisons disease.Acidosis. Medications (in more than 60% )Potassium chloride, heparin, ACE inhibitors, captopril, NSAIDs, and potassium-sparing diuretics.

*Clinical ManifestationsNot significant below a concentration of 7 mEq/L (7 mmol/L), but they are almost always present when the level is 8 mEq/L (8 mmol/L) or greater. Disturbances in cardiac conduction occur. Peaked, narrow T wavesST-segment depression;Shortened QT intervalPR interval becomes prolongeddisappearance of the P waves. decomposition and prolongation of the QRS complex Ventricular dysrhythmias and cardiac arrest Skeletal muscle weakness and even paralysisGI manifestations,Nauseaintermittent intestinal colicdiarrhea

*Medical ManagementAn immediate ECG should be obtained to detect changes. Obtain a repeat serum potassium level from a vein.In non-acute situations;Restriction of dietary potassium and potassium-containing medications may suffice. Administration of either orally or by retention enema, of cation exchange resins (eg, Kayexalate) may be necessary in patients with renal impairment. (Cation in paralytic ileus, hypomagnesemia, hypocalcemia, sodium retention and fluid overload). Administration of bicarbonate and glucose with insulin. 10 to 20 units of regularinsulin and 25 to 50 g of glucose can be used. 10 ml of 10% calcium gluconate to suppress the myocardial effect Enteral administration of cation exchange resign (Kayexalate). Dialysis Avoid exogenous potassium*IV administration of sodium.IV administration of regular insulin and a hypertonic dextrose solution.Beta-2 agonists such as salbutamol, salmeterol, terbutaline, and eformoterol shifts ptassium into the cells.

Calcium chloride and calcium gluconate are not interchangeable: calcium gluconate contains 4.5 mEq of calcium and calcium chloride contains 13.6 mEq of calcium; therefore, caution must be used.

If the hyperkalemic condition is not transient, actual removal of potassium from the body is required; this may be accomplished by using cation exchange resins, peritoneal dialysis, hemodialysis or other forms of renal replacement therapy.

*Nursing ManagementPatients at risk for potassium excess monitored closely for signs of hyperkalemia.Observes for signs of muscle weakness and dysrhythmias. The presence of paresthesias, GI symptoms such as nausea and intestinal colic should be noted.For patients at risk, serum potassium levels are measured periodically.Avoid prolonged use of tourniquet and exercise.Blood sample should be delivered to the laboratory as soon as possible.Preventing hyperkalemiaEncouraging the patient to adhere to the prescribed potassium restriction.Potassium-rich foods to be avoided include coffee, cocoa, tea, dried fruits, dried beans, and wholegrain breads. Conversely, foods with minimal potassium content include butter, margarine, cranberry juice or sauce, ginger ale, gumdrops or jellybeans, hard candy, root beer, sugar, and honey.Correcting hyperkalemiaWhen potassium is added to parenteral solutions, the potassium is mixed with the fluid by inverting the bottle several times. Potassium chloride should never be added to a hanging bottle because the potassium might be administered as a bolus (potassium chloride is heavy and settles to the bottom of the container).Most salt substitutes contain approximately 5060 mEq of potassium per teaspoon.

*significance of calciumMore than 99% of the bodys calcium is located in the skeletal system; it is a major component of bones and teeth. About 1% of skeletal calcium is rapidly exchangeable with blood calcium; the rest is more stable and only slowly exchanged. The small amount of calcium located outside the bone circulates in the serum, partly bound to protein and partly ionized. The normal total serum calcium level is 8.5 to 10.5 mg/dL (2.12.6 mmol/L).It exists in plasma in three forms: Ionized:-About 50% (4.5 to 5.1 mg/dL (1.11.3 mmol/L)) and physiologically active and clinically significant. Bound:-Less than half of the plasma calcium is bound to serum proteins, primarily albumin. The remainder is combined with non-protein anions: phosphate, citrate, and carbonate.Complexed. Calcium is absorbed from foods in the presence of normal gastric acidity and vitamin D. Calcium is excreted primarily in the feces, the remainder in urine.The serum calcium level is controlled by PTH and calcitonin.

*Function;Transmitting nerve impulses Regulate muscle contraction and relaxation, including cardiac muscle.Activating enzymes that stimulate many essential chemical reactions in the body.Blood coagulation.

*A patient may have a total body calcium deficit (as in osteoporosis) but a normal serum calcium level.Elderly people with osteoporosis, who spend an increased amount of time in bed, are at increased risk for hypocalcemia as bed rest increases bone resorption. CausesPrimary hypoparathyroidism Surgical hypoparathyroidism (more common). Massive dministration of citrated blood (transient hypocalcemia).PancreatitisRenal failure Inadequate vitamin D consumption, Magnesium deficiency, Medullary thyroid carcinoma, Low serum albumin levels, Alkalosis Alcohol abuse. Medications (e.g. Aluminum-containing antacids, Aminoglycosides, Caffeine, Cisplatin, Corticosteroids, mithramycin, phosphates, isoniazid, and loop diuretics).

*Clinical ManifestationsTetany (most) Sensations of tingling the tips of the fingers, around the mouth, and less commonly in the feet. Spasms of the muscles of the extremities and face may occur.PainTrousseaus sign (positive)Chvosteks sign (positive)SeizuresMental changes (such as depression, impaired memory, confusion, delirium, and even hallucinations. A prolonged QT interval Prolonged ST segment

*Assessment and Diagnostic FindingsDetermination of serum calcium level, by this formula as follows;Arterial blood gas analaysis.Determination of serum albumin level. For every decrease in serum albumin of 1 g/dL below 4 g/dL, the total serum calcium level is underestimated by approximately 0.8 mg/dL.

*Medical ManagementAcute symptomatic hypocalcemia is life-threatening and requires prompt treatment with IV administration of calcium. Parenteral calcium salts include IV Calcium gluconate (10ml of 10% solution over 10 minute), calcium chloride, and calcium gluceptate. Vitamin D therapyAluminum hydroxide, calcium acetate, or calcium carbonate antacids.For the patient with chronic renal failure. Increasing the dietary intake of calcium to at least 1,000 to 1,500 mg/day in the adult is recommended (eg, milk products; green, leafy vegetables; canned salmon; sardines; fresh oysters).

*Nursing ManagementObserve for hypocalcemia in patients at risk.Seizure precautions.Health education about;Adequate dietary calcium intake, calcium supplements (for peoples risk for osteoporosis) Regular weight-bearing exercise Effect of medications (alcohol, caffeine, cigarette smoking, alendronate (Fosamax), risedronate (Actonel), raloxifene (Evista), and calcitonin).Teaching also addresses strategies to reduce risk for falls.

*Excess of calcium in the plasma.It is a dangerous imbalance when severe.Hypercalcemic crisis has a mortality rate as high as 50% if not treated promptly.The more severe symptoms tend to appear when the serum calcium level is approximately 16 mg/dL (4 mmol/L) or above. However, some patients become profoundly disturbed with serum calcium levels of only 12 mg/dL (3 mmol/L).

*Cardiac standstill (18 mg/dL (4.5 mmol/L))

Excessive urinationAbdominal distentionParalytic ileus Severe thirstPeptic ulcer disease like symptoms.Confusion, Impaired memoryslurred speech,lethargyAcute psychotic behavior,Coma Hypercalcemic crisis refers to an acute rise in the serum calcium level to 17 mg/dL (4.3 mmol/L) or higher.It has the same clinical presentation with varying degree.

Deep Hypothermic Circulatory Arrest is a surgical technique that involves cooling the body of the patient and stopping blood circulation. It is used in cardiac surgery to allow operation on the aortic arch and in neurosurgery to repair some brain aneurysms. ...

*Assessment and Diagnostic FindingsThe serum calcium level is greater than 10.5 mg/dL (2.6 mmol/L).ECG changes;shortening of the QT interval and ST segment. PR interval is sometimes prolonged. The double-antibody PTH test.X-rays The Sulkowitch urine test

The Sulkowitch test measures the amount of calcium excreted in the urine which provides insight on how well the body is able to absorb and utilize dietary calcium.*Medical ManagementGeneral measuresAdministering fluids to dilute serum calcium and promote its excretion by the kidneys.Mobilizing the patient.Restricting dietary calcium intake.Pharmacologic therapyIV administration of 0.9% sodium chloride solution.Administering IV phosphate.Furosemide (Lasix)

*For patients with cancer;surgery, chemotherapy, or radiation therapy.

*Nursing ManagementMonitor the patients at risk. Encourage hospitalized patient to move.Fluids containing sodium should be administered unless contraindicated.Patients are encouraged to drink 3 to 4 quarts of fluid daily. Adequate fiber should be provided in the diet.Safety precautions are taken, as necessary, when mental symptoms of hypercalcemia are present. The patient and family are informed that these mental changes are reversible with treatment. Assess for signs and symptoms of digitalis toxicity. Cardiac rate and rhythm are monitored for any abnormalities.

**Acid; A solution with a higher concentration of hydrogen ions than hydroxide ions.An acid separates into one or more hydrogen ions and one or more negative ions.Base;A solution with a higher concentration of hydroxide ions than hydrogen ions.A base separates into one or more hydroxide ions and one or more positive ions.

*pH;The unit of measurement used to describe the alkalinity or acidity of a substance.It stands for the potential of hydrogen.Measured on a scale 0-14.Scale represents the hydrogen ion concentration.Normal Blood pH is 7.35 7.45.As the value or pH decreases, the hydrogen ion concentration increases and therefore the acidity increases.As the value or pH increases, the hydrogen ion concentration decreases and therefore the acidity decreases.

*PCO2 below the normal range of 31 42 mmHg)* Loss of acid from the stomach by repeated vomiting or aspiration Excessive ingestion of absorbable alkali Hypokalemic alkalosis in patients with pyloric stenosis: potassium loss due to repeated vomiting.*Cheyne-stokes respiration with periods of apnea*Anaerobic tissue metabolism (shock, infection, tissue injury)Chronic diarrhea, gastro colic or high intestinal fistula, excess intestinal aspiration*HeadacheDrowsinessHypotension GI distention

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