Ch 4 Fluid and Electrolyte

Hyperchloremia (Chloride Excess)

Hyperchloremia exists when serum lvl of chloride exceeds 108 mEq/L

Hypercalcemia: Pathophysiology

-90% of hypercalcemia cases are related to either malignancy or hyperparathyroidism. -Considered an oncological emergency, hypercalcemia occurs in 10% to 20% of pts w/ advanced cancer -Associated w/ increased osteoclast activity resulting in bone demineralization and/or tumor-produced factors that affect bone resorption and/or tubular calcium reabsorption. -Tumor cells can secrete PTH-related protein, resulting in increased serum calcium. Excessive PTH secretion associated w/ hyperparathyroidism causes increased release of calcium from the bones & increased intestinal & renal absorption of calcium. -Calcifications of soft tissue occur when calcium-phosphorus product (serum calcium × serum phosphorus) exceeds 70 mg/dL. -Bone mineral is lost during immobilization, & sometimes this causes elevation of total (& esp ionized) calcium in the bloodstream. -Symptomatic hypercalcemia from immobilization is rare; when it does occur, it is virtually limited to ppl w/ high calcium turnover rates. -Most cases of hypercalcemia secondary to immobility occur after severe or multiple fractures or spinal cord injury. -Thiazide diuretics can cause slight elevation in serum calcium lvls b/c they potentiate the action of PTH on the kidneys, reducing urinary calcium excretion. -A rare condition, called milk-alkali syndrome has occurred in pts w/ peptic ulcer treated previously for a prolonged period w/ milk & alkaline antacids, particularly calcium carbonate. -Vit A and D intoxication, as well as use of lithium, can cause calcium excess.

Hypermagnesemia: Clinical Manifestations and Assessment

-Acute elevation of serum mg lvl depresses the CNS as well as the peripheral neuromuscular junction. -At mildly increased lvls, there is a tendency for lowered BP b/c of peripheral vasodilation. Nausea, vomiting, weakness, soft tissue calcifications, facial flushing, & sensations of warmth may also occur. -At higher concentrations, lethargy, difficulty speaking, & drowsiness can occur. Deep tendon reflexes are lost, & muscle weakness & paralysis may develop. -Resp center depressed when serum mg lvls exceed 10 mEq/L. Coma, atrioventricular heart block, & cardiac arrest can occur when serum mg lvl is greatly elevated & not treated. -High lvls also result in platelet clumping & delayed thrombin formation. On lab analysis, serum mg lvl is greater than 2.5 mEq/L or 3.0 mg/dL. -Increased potassium & calcium are present concurrently.

Hypocalcemia: Medical Management

-Acute symptomatic hypocalcemia is life-threatening & requires prompt treatment w/ IV admin of calcium. -Although calcium chloride produces a significantly higher ionized calcium lvl than does calcium gluconate, its not used as often b/c it is more irritating & can cause sloughing of tissue if it infiltrates. -Administering IV calcium too rapidly can cause cardiac arrest, preceded by bradycardia. -IV admin of calcium is particularly dangerous in pts receiving digitalis-derived meds, b/c calcium ions exert an effect similar to that of digitalis & can cause digitalis toxicity, w/ adverse cardiac effects. Therefore, calcium should be diluted in D5W & administered via a slow IV infusion using a volumetric infusion pump. -IV site must be observed often for any evidence of infiltration b/c of risk of extravasation & resultant cellulitis or necrosis. -0.9% sodium chloride solution should not be used w/ calcium because it increases renal calcium loss. -Solutions containing phosphates or bicarbonate should not be used with calcium because they cause precipitation when calcium is added. -Nurse must clarify w/ provider which calcium salt to administer, b/c calcium gluconate yields 4.5 mEq of calcium, & calcium chloride provides 13.6 mEq of calcium. -B/c calcium can cause postural hypotension, pt is kept in bed during IV replacement, & BP is monitored. -Vit D therapy may be instituted to increase calcium absorption from the GI tract. -Aluminum hydroxide, calcium acetate, or calcium carbonate antacids may be prescribed to decrease elevated phosphorus lvls before treating hypocalcemia in pt w/ chronic renal failure. -Increasing dietary intake of calcium to at least 1,000 to 1,500 mg/day is recommended; calcium-containing foods include milk products; green, leafy vegetables; canned salmon; sardines; & fresh oysters. -Hypomagnesemia can also cause tetany; if tetany does not respond to IV calcium, then a low magnesium lvl is considered as a possible cause.

Hyperchloremia: Pathophysiology

-B/c chloride has an affinity for sodium & an inverse relationship w/ bicarbonate, hyperchloremia is related to hypernatremia, bicarbonate loss, & metabolic acidosis. -Hyperchloremic metabolic acidosis is also known as normal anion gap acidosis. Usually caused by the loss of bicarbonate ions via the kidney or GI tract w/ a corresponding increase in chloride ions. Chloride ions in the form of acidifying salts accumulate & acidosis occurs w/ a decrease in bicarbonate ions. -Hyperchloremia results from increased intake either by mouth or by hypertonic IV fluid administration. It can also result from decreased chloride loss as in hyperparathyroidism, hyperaldosteronism, & renal failure

Hypochloremia: Clinical Manifestations and Assessment

-B/c hypochloremia rarely occurs in the absence of other abnormalities, S/S of hypochloremia are associated w/ hyponatremia, hypokalemia, & metabolic alkalosis. -Metabolic alkalosis is a disorder that results in a high pH & a high serum bicarbonate lvl as a result of excess alkali intake or loss of hydrogen ions. -W/ compensation, the partial pressure of carbon dioxide in arterial blood (PaCO2) increases to 50 mm Hg. Hyperexcitability of muscles, tetany, hyperactive deep tendon reflexes, weakness, twitching, & muscle cramps may result. -Hypokalemia can cause hypochloremia, resulting in cardiac arrhythmias. In addition, b/c low chloride lvls parallel low sodium lvls, a water excess may occur. Hyponatremia can cause seizures & coma. -In addition to the chloride lvl, sodium & potassium lvls are also evaluated, b/c these electrolytes are lost along w/ chloride. -Arterial blood gas analysis identifies the acid-base imbalance, which is usually metabolic alkalosis. Urine chloride lvl, which is also measured, decreases in hypochloremia

Monitoring Flow

-B/c so many factors influence gravity flow, a solution does not necessarily continue to run at speed originally set. Nurse monitors IV infusions freq to make sure the fluid is flowing at intended rate. -IV container should be marked w/ tape to indicate at a glance whether the correct amount has infused. -Flow rate is calculated when the solution is originally started & then monitored at least hourly. To calculate flow rate, the nurse determines # of drops delivered per mL; varies w/ equipment & is usually printed on administration set packaging. -In an effort to decrease the amount of med errors, it has become standard for all intermittent IV infusions to be given w/ an electronic infusion device. These devices allow more accurate admin of fluids & meds than is possible w/ routine gravity-flow setups. -A pump is a positive-pressure device that uses pressure to infuse fluid at a pressure of 10 psi; newer models use a pressure of 5 psi. The pressure exerted by the pump overrides vascular resistance (increased tubing length, low height of the IV container). -Volumetric pumps calculate the volume delivered by measuring the volume in a reservoir that is part of the set & is calibrated in mL/h. -Controller is an infusion assist device that relies on gravity for infusion; volume is calibrated in drops (gtt) per min. Uses a drop sensor to monitor the flow. -Factors essential for safe use of pumps include alarms to signify the presence of air in the IV line or an occlusion. -The standard for the accurate delivery of fluid or med via an electronic IV infusion pump is plus or minus 5% -Use of these devices does not eliminate need for the nurse to monitor the infusion & the pt freq; however, it does limit the amount of bedside drug calculations & med administration errors. -Flushing of a vascular device is performed to ensure patency & to prevent mixing of incompatible meds or solutions. This procedure should be carried out at established intervals, according to hospital policy & procedure, esp for intermittently used catheters. -Most manufacturers & researchers suggest use of saline for flushing. Volume of the flush solution should be at least twice the volume capacity of the cath. -Cath should be clamped before the syringe is completely empty & withdrawn to prevent reflux of blood into the lumen, which could cause cath clotting & infiltration.

Hypomagnesemia: Nursing Management

-Be aware of pts who are at risk for hypomagnesemia & observe them for its S/S. -Patients receiving digitalis are monitored closely b/c a deficit of mg can predispose them to digitalis toxicity. -If hypomagnesemia severe, seizure precautions are implemented. Other safety precautions are instituted if confusion observed. -B/c difficulty in swallowing may occur in magnesium-depleted pts, a nursing swallowing evaluation should be performed before oral meds or foods offered. Dysphagia probably related to the athetoid or choreiform (rapid, involuntary, & irregular jerking) movements associated w/ mg deficit. -To determine neuromuscular irritability, nurse needs to assess & grade deep tendon reflexes. -Teaching plays a major role in treating mg deficit, particularly that resulting from abuse of diuretic or lax meds. In such cases, nurse instructs pt about the need to consume magnesium-rich foods. -Pts experiencing hypomagnesemia from abuse of alcohol, nurse provides teaching, counseling, support, & possible referral to alcohol abstinence programs or other professional help.

Preparing to Administer IV Therapy

-Before performing venipuncture, nurse performs hand hygiene, applies gloves, & informs pt about the procedure. -Nurse then selects the most appropriate insertion site & type of cannula for a particular pt. -Factors influencing these choices include the type of solution to be administered, expected duration of IV therapy, the pt's general condition, & availability of veins. -The skill of the person initiating the infusion is also an important consideration.

Hyperchloremia: Medical Management

-Correcting underlying cause of hyperchloremia & restoring electrolyte, fluid, & acid-base balance are essential. -Hypotonic IV solutions may be given to restore balance. -Lactated Ringer's solution may be prescribed to convert lactate to bicarbonate in the liver, which increases the base bicarbonate lvl & corrects the acidosis. -IV sodium bicarbonate may be administered to increase bicarbonate lvls, which leads to the renal excretion of chloride ions as bicarbonate & chloride compete for combination w/ sodium. -Diuretics may be administered to eliminate chloride as well. Sodium, chloride, & fluids are restricted

Teaching the Patient: Preparing the IV Site

-Before preparing the skin, nurse should ask pt whether he or she is allergic to latex or iodine, products commonly used in preparing for IV therapy. -Excessive hair at selected site may be removed by clipping to increase visibility of the veins & to facilitate insertion of the cannula & adherence of dressings to the IV insertion site. Shaving should not be performed due to increased risk of infection. -B/c infection can be a major complication, the IV device, fluid, container, & the tubing must be sterile. -Insertion site is scrubbed w/ a sterile pad soaked in 10% povidone-iodine (Betadine) or chlorhexidine gluconate solution for 30 secs, working in a circular motion from the center of the area to the periphery & allowing the area to air dry for approx 2 mins. -Site should not be wiped w/ 70% alcohol, b/c the alcohol negates the effect of the disinfecting solution. (Alcohol pledgets used for 30 secs instead, only if pt is allergic to iodine) -Nurse must perform hand hygiene & put on gloves. Gloves must be worn during the venipuncture procedure b/c of the likelihood of coming into contact w/ the pt's blood

Hypochloremia (Chloride Deficit)

-Chloride control depends on the intake of chloride & the excretion & reabsorption of its ions in the kidneys. -Chloride is produced in the stomach, where it combines w/ hydrogen to form hydrochloric acid. -A small amount of chloride is lost in the feces. GI tube drainage & severe vomiting & diarrhea, lax, ileostomy, & fistulas are risk factors for hypochloremia. -Admin of chloride-deficient formulas, low sodium intake, decreased serum sodium levels, metabolic alkalosis, prolonged therapy w/ IV dextrose, diuretic therapy, burns, & fever may also cause hypochloremia. -As chloride decreases (usually b/c of volume depletion), sodium & bicarbonate ions are retained by the kidney to balance the loss. Bicarbonate accumulates in the ECF, which raises the pH & leads to hypochloremic metabolic alkalosis

Chloride Imbalances

-Chloride, the major anion of the ECF, is found more in interstitial & lymph fluid compartments than in blood. Chloride is also contained in gastric & pancreatic juices, sweat, bile, & saliva. -Choroid plexus, where CSF forms in the brain, depends on sodium & chloride to attract water to form the fluid portion of the CSF. -Sodium & chloride in water make up the composition of the ECF & assist in determining osmotic pressure. -Serum lvl of chloride reflects a change in dilution or concentration of the ECF & does so in direct proportion to the sodium concentration. Serum osmolality parallels chloride lvls as well. -The normal serum chloride lvl is 100 to 108 mEq/L. Inside the cell, the chloride lvl is 4 mEq/L. -Plasma bicarbonate has an inverse relationship w/ chloride. For ex. the carbonic anhydrase reaction in RBCs generates both hydrogen & bicarbonate from metabolically produced CO2. Hydrogen facilitates the dissociation of oxygen from hemoglobin. The intracellular accumulation of bicarbonate is prevented by its movement out of the cell into the plasma. To maintain electrical neutrality, chloride enters the RBC, a response referred to as the chloride shift. -Important to note that when the lvl of one of these three electrolytes (sodium, bicarbonate, or chloride) is disturbed, the other two are also affected. -Chloride is important not only in maintaining acid-base balance, but it also mediates the hyperpolarizing effect of many neurotransmitters on the membrane potential. Chloride is primarily obtained from the diet as table salt

Parental Fluid Therapy: Purpose

-Choice of IV solution depends on purpose of its administration. -Generally, IV fluids administered to achieve one or more of the following goals: (1) To provide water, electrolytes, & nutrients to meet daily requirements, (2) to replace water & correct electrolyte deficits, & (3) to administer meds & blood products -IV solutions contain dextrose or electrolytes mixed in various proportions w/ water. Pure, electrolyte-free water can never be administered IV b/c it rapidly enters RBC & causes them to rupture.

Hypomagnesemia: Clinical Manifestations and Assessment

-Clinical manifestations are largely confined to the neuromuscular sytm. -Some effects are due directly to the low serum mg lvl; others are due to secondary changes in potassium & calcium metabolism. -Symptoms do not usually occur until serum mg lvl has dropped to less than 1 mEq/L. -Among the neuromuscular changes are hyperexcitability w/ muscle weakness, tremors, & athetoid movements (slow, involuntary twisting & writhing). Others include tetany, generalized tonic-clonic or focal seizures, laryngeal stridor, & positive Chvostek's & Trousseau's signs, which occur, in part, b/c of accompanying hypocalcemia. -Hypomagnesemia may be accompanied by marked alterations in mood. Apathy, depression, apprehension, & extreme agitation have been noted, as well as ataxia, dizziness, insomnia, & confusion. At times, delirium, auditory or visual hallucinations, & frank psychoses may occur. -On lab analysis, serum mg lvl is less than 1.3 mEq/L or 1.8 mg/dL. -Hypomagnesemia is freq associated w/ hypokalemia & hypocalcemia. -About 25% of mg is protein-bound, principally to albumin. Decreased serum albumin lvl can, therefore, reduce the measured total mg concentration. -Torsades de pointes is associated w/ a low mg lvl. Premature ventricular contractions, paroxysmal atrial tachycardia, & heart block may also occur. -Digitalis toxicity is associated w/ low serum mg lvls. This is important, b/c pts receiving digoxin are also likely to be receiving diuretic therapy, predisposing them to renal loss of mg. -Urine magnesium lvls may be helpful in identifying causes of magnesium depletion & are measured after loading dose of mg sulfate is administered.

Hypomagnesemia: Pathophysiology

-Common yet often overlooked imbalance in acutely & critically ill pts. -May occur w/ withdrawal from alcohol & administration of tube feedings or parenteral nutrition. -An important route of mg loss is the GI tract. Loss of magnesium from GI tract may occur w/ nasogastric suction, diarrhea, or fistulas. -B/c fluid from lower GI tract has a higher concentration of mg (10 to 14 mEq/L) than fluid from the upper tract (1 to 2 mEq/L), losses from diarrhea & intestinal fistulas are more likely to induce mg deficit than those from gastric suction. -Although mg losses are relatively small in nasogastric suction, hypomagnesemia will occur if losses are prolonged & mg is not replaced through IV infusion. -B/c the distal small bowel is the major site of mg absorption, any disruption in small-bowel function (intestinal resection or inflammatory bowel disease) can lead to hypomagnesemia. -Hypomagnesemia is particularly troublesome during treatment of alcohol withdrawal. Therefore, serum magnesium lvl should be routinely measured in pts undergoing withdrawal from alcohol. Serum mg level may be normal on admission but may decrease as result of metabolic changes, such as the intracellular shift of mg associated w/ IV glucose administration. -During nutritional replacement, the major cellular electrolytes move from the serum to newly synthesized cells. -Pts on enteral or parenteral feedings should have mg lvls routinely measured as serious hypomagnesemia can occur w/ magnesium-deficient formulas, esp in those who have undergone a period of starvation. -Other causes of hypomagnesemia include the administration of aminoglycosides, cyclosporine, cisplatin, diuretics, digitalis, & amphotericin, & the rapid administration of citrated blood, esp to pts w/ renal or hepatic disease. -Magnesium deficiency often occurs in diabetic ketoacidosis, secondary to increased renal excretion during osmotic diuresis and shifting of magnesium into the cells w/ insulin therapy. -Other contributing causes are sepsis, burns, & hypothermia.

Types of IV Solutions (Table 4-6)

-Crystalloid solutions are often categorized as isotonic, hypotonic, or hypertonic, according to whether their total osmolality is the same as, less than, or greater than that of blood. -Crystalloid fluids generally contain 3 basic components: water, electrolytes, & sugar. -Electrolyte solutions considered isotonic if the total electrolyte content (anions + cations) is approx 310 mEq/L, hypotonic if the total electrolyte content is less than 250 mEq/L, & hypertonic if the total electrolyte content is greater than 375 mEq/L. -Nurse must also consider a solution's osmolality, keeping in mind that the osmolality of plasma is approximately 300 mOsm/L (300 mmol/L). For ex, a 10% dextrose solution has an osmolality of approx 505 mOsm/L. -When administering parenteral fluids, nurse monitors pt's response to the fluids, considering the fluid volume, the content of the fluid, & the pt's clinical status. -Some fluids may actually initiate an inflammatory process within the body, esp when overused in pts w/ hemorrhage shock. ** When administering fluids to pts w/ cardiovascular disease, the nurse assess for signs of circulatory overload (cough, dyspnea, puffy eyelids, dependent edema, wgt gain in 24 hrs). Extreme care is taken when administering highly hypertonic sodium fluids ( 3 or 5% sodium chloride) b/c these fluids can be lethal if infused carelessly.**

Teaching the Patient

-Except in emergency situations, a pt should be prepared in advance for an IV infusion. -Venipuncture, expected length of infusion, & activity restrictions are explained. -Pt should have an opportunity to ask questions & express concerns.

Hypocalcemia: Pathophysiology

-Factors associated w/ hypocalcemia include inadequate calcium intake, increased calcium loss, malabsorption of calcium, decreases in serum protein lvls, & increased binding of calcium. -Inadequate intake is associated w/ chronic alcoholism & malnutrition. -Increased calcium loss is associated w/ pancreatic insufficiency & acute pancreatitis. -Inflammation of pancreas causes the breakdown of proteins & lipids. It is thought that calcium ions combine w/ the fatty acids released by lipolysis, forming soaps. As a result of this process, hypocalcemia occurs & is common in pancreatitis. - Has also been suggested that hypocalcemia might be related to excessive secretion of glucagon from the inflamed pancreas, which results in increased secretion of calcitonin (hormone that lowers serum calcium). -Inadequate secretion of PTH by parathyroid gland results in hypocalcemia & can be related to hypoparathyroidism or other parathyroid gland disorders, use of certain drugs, surgery of the thyroid gland w/ inadvertent removal of the parathyroids, radiation injury to thyroid, & radical neck dissection. This is likely to occur in first 24 to 48 hours postoperatively. -Meds predisposing to hypocalcemia include aluminum-containing antacids, aminoglycosides, anticonvulsants, corticosteroids, mithramycin, phosphates, isoniazid, & loop diuretics. -Malabsorption of calcium may be seen in severe diarrhea, lax abuse, decreased exposure to sunlight or conditions that impair vit D, high phosphorus level in intestines, reduced gastric acidity, & renal failure. -Hypoalbuminemia, alkalosis, & massive blood transfusion are associated w/ hypocalcemia. - Decrease in serum albumin will result in a decrease in total serum calcium, but it does not affect concentration of the ionized form of calcium that is essential for body function. -When arterial pH increases (alkalosis), more calcium becomes bound to protein. As a result, the ionized portion decreases, thus symptoms of hypocalcemia may occur w/ alkalosis. -Transient hypocalcemia can occur w/ massive admin of citrated blood (adults who experience massive hemorrhage & shock), b/c citrate (which is used in blood transfusions to prevent clotting in blood) can combine w/ ionized calcium & temporarily remove it from circulation.

Understanding Factors Affecting Flow

-Flow of an IV infusion is governed by the same principles that govern fluid movement in general. Flow is directly proportional to the height on the infusion. -Raising infusion bag may improve sluggish flow. The clamp on IV tubing regulates flow by changing the tubing diameter. The flow is faster through large-gauge rather than small-gauge cannulas. -Issues such as length of IV tubing & viscosity of the fluid being infused may also affect the flow rate

Hypermagnesemia: Medical Management

-Hypermagnesemia can be prevented by avoiding administration of mg to pts w/ renal failure & by carefully monitoring seriously ill pts who are receiving mg salts. -In pts w/ severe hypermagnesemia, all parenteral & oral mg salts discontinued. -In emergencies, such as resp depression or defective cardiac conduction, ventilatory support & IV calcium gluconate are indicated. -In addition, hemodialysis w/ a magnesium-free dialysate can reduce serum mg to a safe lvl within hrs. -Administration of loop diuretics (Lasix) & sodium chloride or lactated Ringer's IV solution enhances mg excretion in pts w/ adequate renal function. -IV calcium gluconate antagonizes the cardiovascular & neuromuscular effects of mg

Hypermagnesemia (Magnesium Excess)

-Hypermagnesemia is a rare electrolyte abnormality b/c the kidneys are efficient in excreting magnesium. -A serum mg lvl can appear falsely elevated if blood specimens are allowed to hemolyze or are drawn from extremity w/ a tourniquet that was applied too tightly or for too long a period of time prior to blood draw

Hypomagnesemia (Magnesium Deficit)

-Hypomagnesemia refers to a below-normal serum magnesium concentration (1.3 to 2.3 mEq/L; 1.8 to 3.0 mg/dL; 0.8 to 1.2 mmol/L). -Magnesium similar to calcium in two aspects: (1) it is the ionized fraction of mg that is primarily involved in neuromuscular activity & other physiologic processes, & (2) mg lvls should be evaluated in combination w/ albumin lvls. Low serum albumin lvls decrease total magnesium.

Hypophosphatemia (Phosphorous Deficit): Pathophysiology

-Hypophosphatemia is a below-normal serum concentration of inorganic phosphorus; may occur under a variety of circumstances in which total body phosphorus stores are normal. -Phosphorus deficiency is an abnormally low content of phosphorus in lean tissues that may exist in the absence of hypophosphatemia. -Can be caused by an intracellular shift of potassium from serum into cells, by increased urinary excretion of potassium, or by decreased intestinal absorption of potassium. -Hypophosphatemia may occur during admin of calories to pts w/ severe protein-calorie malnutrition. Most likely to occur w/ overzealous intake or administration of simple carbs. This syndrome can be induced in anyone w/ severe protein-calorie malnutrition, such as pts w/ anorexia nervosa -Approx 50% of patients hospitalized due to chronic alcoholism have hypophosphatemia. -Marked hypophosphatemia may develop in malnourished pts who receive parenteral nutrition if phosphorus loss is not adequately corrected. -Other causes include pain, heat stroke, prolonged intense hyperventilation, alcohol withdrawal, poor dietary intake, diabetic ketoacidosis, hepatic encephalopathy, & major thermal burns. -Low magnesium lvls, low potassium lvls, & hyperparathyroidism related to increased urinary losses of phosphorus contribute to hypophosphatemia. -Loss of phosphorus through the kidneys also occurs w/ acute volume expansion, osmotic diuresis, use of carbonic anhydrase inhibitors (acetazolamide), & some malignancies. -Resp alkalosis can cause decrease in phosphorus b/c of intracellular shift of phosphorus, which often stimulates intracellular glycolysis. -Excess phosphorus binding by antacids containing magnesium, calcium, or albumin may decrease phosphorus available from the diet to an amount lower than required to maintain serum phosphorus balance. -Degree of hypophosphatemia depends on amount of phosphorus in the diet compared to the dose of antacid. -Phosphate loss can occur w/ chronic diarrhea or through severe potassium restriction. -Vit D regulates intestinal ion absorption; therefore, a deficiency of vit D may cause decreased calcium & phosphate (phosphorus) lvls, which may lead to osteomalacia (softened, brittle bones).

Performing Ventipuncture

-IV therapy initiation is a specialized nursing skill. Institutional policies & procedures determine whether all nurses must be certified to perform venipuncture. -Nurse certified in IV therapy or an IV team can be consulted to assist w/ initiating IV therapy.

Hypocalcemia: Clinical Manifestations and Assessment &

-If ionized calcium lvl is normal despite low total calcium levels, pts are generally asymptomatic, whereas large changes in ionized calcium levels leads to variety of symptoms associated w/ neuromuscular hyperactivity & cardiovascular effects. -Tetany (most characteristic manifestation) & convulsions are seen when total calcium level is less than 4.4 mg/dL, and/or the ionized calcium is less than 2.0 mg/dL. -Tetany refers to the entire symptom complex induced by increased neural excitability. Symptoms are caused by spontaneous discharges of sensory & motor fibers in peripheral nerves. Sensations of tingling may occur in tips of fingers, around the mouth, &, less commonly, in the feet. -Spasms of the muscles of the extremities & face may occur. Pain may develop as a result of these spasms. -Trousseau's sign can be elicited by inflating BP cuff on the upper arm to about 20 mm Hg above systolic pressure; within 2 to 5 mins, carpal spasm (an adducted thumb, flexed wrist & metacarpophalangeal joints, extended interphalangeal joints w/ fingers together) will occur as ischemia of the ulnar nerve develops. -Chvostek's sign consists of twitching of muscles supplied by facial nerve when the nerve is tapped about 2 cm anterior to the earlobe, just below zygomatic arch. -Seizures occur b/c hypocalcemia causes irritability of the CNS as well as of the peripheral nerves. -Other changes associated w/ hypocalcemia include mental changes, such as depression, impaired memory, confusion, delirium, & even hallucinations. -Prolonged QT interval is seen on ECG due to prolongation of ST segment, which predisposes pts to a form of ventricular tachycardia called torsades de pointes. -Respiratory effects w/ include dyspnea & laryngospasm (stridor). -S/S of chronic hypocalcemia include hyperactive bowel sounds, dry & brittle hair & nails, & abnormal clotting. -When evaluating serum calcium lvls, variables such as serum albumin lvl & the arterial pH must be considered. -B/c abnormalities in serum albumin lvls may affect interpretation of serum calcium level, it may be necessary to calculate the corrected serum calcium if serum albumin level is abnormal. For every decrease in serum albumin of 1 g/dL below 4 g/dL, the total serum calcium level is underestimated by approx 0.8 mg/dL. Quick method to calculate corrected serum calcium level: Corrected calcium = measured calcium + 0.8 (4.0 − measured serum albumin) -Ionized calcium lvl is usually normal in pts w/ reduced total serum calcium lvls & concomitant hypoalbuminemia. -Ideally, ionized lvl of calcium should be measured in the lab. However, in many labs, only total calcium lvl is reported; therefore, the concentration of the ionized fraction must be estimated by simultaneous measurement of the serum albumin lvl. -PTH levels & magnesium & phosphorus lvls need to be assessed to identify possible causes of decreased calcium.

Hyperphosphatemia: Clinical Manifestations and Assessment

-Increased serum phosphorus lvl causes few symptoms. Symptoms that do occur usually result from decreased calcium lvls & soft tissue calcifications. -Most important short-term consequence is tetany. B/c of the reciprocal relationship b/w phosphorus & calcium, a high serum phosphate lvl tends to cause a low serum calcium concentration. Tetany can result, causing tingling sensations in fingertips & around the mouth. Anorexia, nausea, vomiting, bone & joint pain, muscle weakness, hyperreflexia, & tachycardia may occur. -Major long-term consequence is soft tissue calcification, which occurs mainly in pts w/ a reduced glomerular filtration rate. High serum lvls of inorganic phosphorus promote precipitation of calcium phosphate in nonosseous sites, decreasing urine output, impairing vision, & producing palpitations. -On lab analysis, serum phosphorus lvl exceeds 4.5 mg/dL. -Serum calcium lvl is useful also for diagnosing the primary disorder & assessing the effects of treatments. -X-ray studies may show skeletal changes w/ abnormal bone development. PTH lvls are decreased in hypoparathyroidism. BUN & creatinine lvls are used to assess renal function. Renal ultrasonography may be indicated as part of diagnostic assessment for renal failure; bone studies & coronary calcification studies also provide info about chronicity & prognosis of renal failure

Hypercalcemia: Nursing Management

-Interventions such as increasing pt mobility & encouraging fluids can help prevent hypercalcemia, or at least minimize its severity. -Fluids containing sodium should be administered unless contraindicated b/c sodium favors calcium excretion. Pts encouraged to drink 3 to 4 quarts of fluid daily. -Adequate fiber should be provided in diet to offset the tendency for constipation. -Safety precautions implemented, as necessary, when mental symptoms of hypercalcemia present. Pt & fam informed that these mental changes are reversible w/ treatment. -Increased calcium potentiates the effects of digitalis; therefore, pt is assessed for S/S of digitalis toxicity. -B/c ECG changes (premature ventricular contractions, paroxysmal atrial tachycardia, & heart block) can occur, cardiac rate & rhythm monitored for any abnormalities.

Types of IV Solutions: Isotonic Fluids

-Isotonic fluids have a total osmolality close to that of the ECF & do not cause RBC to shrink or swell. -Composition of these fluids may or may not approx that of the ECF. -Isotonic fluids expand the ECF volume. One liter of isotonic fluid expands the ECF by 1 L; however, it expands the plasma by only 0.25 L b/c it is a crystalloid fluid & diffuses quickly into the ECF compartment. -In pts hospitalized for shock, as much as 20 mL/kg of isotonic fluid boluses may be initially required to maintain renal perfusion. However, since these fluids expand the intravascular space, pts w/ hypertension & heart failure should be carefully monitored for signs of fluid overload

Managing Local Complications

-Local complications of IV therapy include infiltration & extravasation, phlebitis, thrombophlebitis, hematoma, & clotting of the needle. -Infiltration is the unintentional administration of a nonvesicant solution or med into surrounding tissue. Can occur when the IV cannula dislodges or perforates wall of the vein. Infiltration is characterized by edema around insertion site, leakage of IV fluid from the insertion site, discomfort & coolness in the area of infiltration, & a significant decrease in the flow rate. -When the solution is particularly irritating, sloughing of tissue may result. Close monitoring of the insertion site is necessary to detect infiltration before it becomes severe. -Infiltration is usually easily recognized if insertion area is larger than the same site of the opposite extremity; however, it is not always so obvious. -A common misconception is that a backflow of blood into the tubing proves that the cath is properly placed within the vein. However, if the cath tip has pierced the wall of the vessel, IV fluid will seep into tissues as well as flow into the vein. Although blood return occurs, infiltration has occurred as well. -A more reliable means of confirming infiltration is to apply a tourniquet above (or proximal to) the infusion site & tighten it enough to restrict venous flow. If infusion continues to drip despite the venous obstruction, infiltration is present. -As soon as the nurse notes infiltration, the infusion should be stopped, the IV discontinued, & a sterile dressing applied to the site after careful inspection to determine extent of infiltration. -Infiltration of any amount of blood product, irritant, or vesicant is considered the most severe. -IV infusion should be started in a new site or proximal to infiltration if the same extremity must be used again. -A warm compress may be applied to the site if small volumes of noncaustic solutions have infiltrated over a long period, or if the solution was isotonic w/ a normal pH; affected extremity should be elevated to promote the absorption of fluid. -If infiltration is recent & the solution was hypertonic or had an increased pH, a cold compress may be applied to the area. -Infiltration can be detected & treated early by inspecting the site every hr for redness, pain, edema coolness at the site, & IV fluid leaking from the IV site. -Using appropriate size & type of cannula for the vein prevents this complication. -Extravasation is similar to infiltration, w/ an inadvertent admin of vesicant or irritant solution or med into the surrounding tissue. -Meds such as dopamine, calcium preparations, & chemotherapeutic agents can cause pain, burning, & redness at the site. Blistering, inflammation, & necrosis of tissues can occur. -Extent of tissue damage is determined by the concentration of the med, quantity that extravasated, location of the infusion site, tissue response, & the duration of the process of extravasation. -Infusion must be stopped & provider notified promptly. Agency's protocol to treat extravasation is initiated; protocol may specify specific treatments & may indicate whether IV line should remain in place or be removed before treatment. -The protocol often specifies infiltration of the infusion site w/ an antidote prescribed after assessment by the provider, removal of the cannula, & application of warm compresses to sites of extravasation from vinca alkaloids or cold compresses to sites of extravasation from alkylating & antibiotic vesicants. -Affected extremity should not be used for further cannula placement. Thorough neurovascular assessments of affected extremity must be performed freq. -Reviewing the institution's IV policy & procedures & incompatibility charts & checking w/ the pharmacist before administering any IV meds, whether given peripherally or centrally, is a prudent way to determine incompatibilities & vesicant potential to prevent extravasation. -Careful, freq monitoring of IV site, avoiding insertion of IV devices in areas of flexion, securing the IV line, & using the smallest cath possible that accommodates the vein help minimize the incidence & severity of this complication. -When vesicant med is administered by IV push, it should be given through a side port of an infusing IV solution to dilute the med & decrease the severity of tissue damage if extravasation occurs. -Signs of phlebitis & infiltration may be assessed using a scale such as the Infusion Nurses Society (INS) infiltration scale. Scale ranges from 0, or no edema, to 4, which includes pitting edema, moderate to severe pain at the site, or circulatory impairment. Extravasation should always be rated as a grade 4 on the infiltration scale. -Phlebitis is defined as inflammation of a vein, which can be categorized as chemical, mechanical, or bacterial; however, two or more of these types of irritation often occur simultaneously. -Chemical phlebitis can be caused by an irritating med or solution, rapid infusion rates, & med incompatibilities. -Mechanical phlebitis results from long periods of cannulation, caths in flexed areas, catheter gauges larger than the vein lumen, & poorly secured catheters. -Bacterial phlebitis can develop from poor hand hygiene, lack of aseptic technique, failure to check all equipment before use, & failure to recognize early signs & symptoms of phlebitis. -Other factors include poor venipuncture technique, cath in place for a prolonged period, & failure to adequately secure cath. -Phlebitis is characterized by a reddened, warm area around the insertion site or along the path of the vein, pain or tenderness at the site or along the vein, & swelling. -Incidence of phlebitis increases w/ the length of time IV line is in place, the composition of the fluid or med infused, the size & site of the cannula inserted, ineffective filtration, inadequate anchoring of the line, & the intro of microorganisms at time of insertion. -Treatment consists of discontinuing the IV & restarting it in another site, & applying a warm, moist compress to the affected site. -Phlebitis can be prevented by using aseptic technique during insertion, using appropriate-size cannula or needle for the vein, considering the composition of fluids and meds when selecting a site, observing the site hourly for any complications, anchoring the cannula or needle well, & changing IV site according to agency policy & procedures. -Thrombophlebitis refers to the presence of a clot plus inflammation in the vein. It is evidenced by localized pain, redness, warmth, & swelling around insertion site or along the path of the vein, immobility of the extremity b/c of discomfort & swelling, sluggish flow rate, fever, malaise, & leukocytosis. -Treatment includes discontinuing IV infusion; applying cold compress first, to decrease the flow of blood & increase platelet aggregation, followed by a warm compress; elevating the extremity; & restarting the line in the opposite extremity. -If the pt has S/S of thrombophlebitis, the IV line should not be flushed. Cath must be removed promptly. -In some circumstances, the cath tip may be sent to the lab for culture, & it should be removed & placed in a sterile container prior to sending to the lab. -Thrombophlebitis can be prevented by avoiding trauma to the vein at the time IV is inserted, observing the site every hr, & checking med additives for compatibility. -Hematoma results when blood leaks into tissues surrounding IV insertion site. Leakage can result if the opposite vein wall is perforated during venipuncture, the needle slips out of the vein, or insufficient pressure is applied to the site after removal of the needle or cannula. Signs of a hematoma include ecchymosis, immediate swelling at the site, & leakage of blood at the insertion site. -Treatment includes removing the needle or cannula & applying light pressure w/ a sterile, dry dressing; applying ice for 24 hrs to the site to avoid extension of the hematoma; elevating the extremity; assessing the extremity for any circulatory, neurologic, or motor dysfunction; & restarting the line in the other extremity if indicated. -Hematoma can be prevented by carefully inserting the needle & by using diligent care w/ pts who have a bleeding disorder, are taking anticoagulant med, or have advanced liver disease. -Blood clots may form in the IV line as a result of kinked IV tubing, a very slow infusion rate, an empty IV bag, or failure to flush the IV line after intermittent med or solution administrations. -The signs are decreased flow rate & blood backflow into IV tubing. If blood clots in the IV line, infusion must be discontinued & restarted in another site w/ a new cannula & admin set. -Tubing should not be irrigated or milked. Neither the infusion rate nor the solution container should be raised, & the clot should not be aspirated from the tubing. -Clotting of the needle or cannula may be prevented by not allowing the IV solution bag to run dry, taping the tubing to prevent kinking & maintain patency, maintaining an adequate flow rate, & flushing the line after intermittent med or other solution admin.

Magnesium Imbalances

-Magnesium is the most abundant intracellular cation after potassium. It acts as an activator for many intracellular enzyme systems & plays a role in both carbohydrate & protein metabolism. -The normal serum magnesium lvl is 1.3 to 2.3 mEq/L. -Approx one-third of serum magnesium is bound to protein; remaining two thirds exists as free cations—the active component (Mg++). -Mg balance important in neuromuscular function. B/c magnesium acts directly on the myoneural junction, variations in the serum concentration of mg affect neuromuscular irritability & contractility. -Mg produces its sedative effect at the neuromuscular junction, probably by inhibiting release of the neurotransmitter acetylcholine. -Mg exerts effects on the cardiovascular system, acting peripherally to produce vasodilation. -Mg is thought to have a direct effect on peripheral arteries & arterioles, which results in a decreased total peripheral resistance. -IV mg may also be helpful in pts w/ acute asthma by potentially improving both bronchodilation & airflow. -Mg predominantly found in bone & soft tissues & primarily eliminated by the kidneys.

Hypomagnesemia: Medical Management

-Mild mg deficiency can be corrected by diet alone. Principal dietary sources of mg are green leafy vegetables, nuts, seeds, legumes, whole grains, & seafood. Mg also plentiful in peanut butter & cocoa. -If necessary, magnesium salts can be administered orally in an oxide or gluconate form to replace continuous excessive losses. -Diarrhea is a common complication of excessive ingestion of mg. -Pts receiving parenteral nutrition require mg in IV solution to prevent hypomagnesemia. -Mg sulfate must be administered intravenously by infusion pump typically at rate of 1 to 2 grams over an hour. Bolus dose of mg sulfate given too rapidly can produce alterations in cardiac conduction leading to heart block or asystole. -Vital signs must be assessed freq during mg administration to detect changes in cardiac rate or rhythm, hypotension, & respiratory distress. -Monitoring urine output essential before, during, & after mg administration; provider is notified if urine volume decreases to less than 100 mL over 4 hrs. -Calcium gluconate must be readily available to treat hypocalcemic tetany or hypermagnesemia. -Overt symptoms of hypomagnesemia are treated w/ parenteral administration of mg. Mg sulfate is most commonly used mg salt. Serial measurements of serum mg lvls can be used to regulate the dosage.

Hyperchloremia: Nursing Management

-Monitoring vital signs, ABG values, & patient's I&O status is important to assess the pt's status & the effectiveness of treatment. -Assessment findings related to respiratory, neurologic, & cardiac systems are documented, & changes discussed w/ the provider. -Nurse teaches the pt about diet that should be followed to manage hyperchloremia & maintain adequate hydration

Calcium Imbalances

-More than 99% of body's calcium is located in the skeletal system, where it provides strength & stability to the skeletal system & serves as a source for extracellular calcium. -Approx 0.1% to 0.2% of calcium circulates in the serum, 40% is bound to plasma proteins (mostly albumin), 10% is complexed or chelated w/ substances such as phosphorus & sulfate, & approx 50% is ionized or free to leave blood stream & participate in cellular function. -Calcium plays major role in transmitting nerve impulses & helps regulate muscle contraction & relaxation, including cardiac muscle; thus, it is important for cardiac conduction, neuromuscular activity, & blood coagulation. -Calcium is also instrumental in activating enzymes that stimulate many essential chemical reactions in the body. -B/c many factors affect calcium regulation, hypocalcemia & hypercalcemia are relatively common disturbances. -Calcium is absorbed from foods (milk & milk products) in the presence of normal gastric acidity & vit D & is excreted in feces & urine. -Serum calcium lvl is controlled by PTH & calcitonin. As ionized or free serum calcium decreases, parathyroid glands secrete PTH. This increases calcium absorption from the GI tract (mediated by increase in renal vit D synthesis), increases calcium reabsorption from the renal tubule, & releases calcium from the bone. The subsequent increase in calcium ion concentration suppresses PTH secretion. When calcium increases excessively, thyroid gland secretes calcitonin, the antagonist of PTH. It briefly inhibits calcium reabsorption from bone, encourages calcium salt deposits in the bone matrix, & decreases serum calcium concentration. -Blood phosphate (most phosphorus is present as phosphate) lvls have a reciprocal relationship w/ calcium levels. Increases in blood phosphate result in a fall in free calcium concentrations. PTH secretion is stimulated, & this reduces renal excretion of calcium & increases renal phosphate excretion. -These adaptations prevent potentially damaging effects of calcium phosphate crystal deposition that can form in soft tissues when normal calcium phosphorus ratio is disturbed.

Hypermagnesemia: Pathophysiology

-Most common cause of hypermagnesemia is renal failure. Most pts w/ advanced renal failure have at least a slight elevation in serum mg lvls. -This condition is aggravated when such pts receive mg to control seizures or inadvertently take one of the many commercial antacids that contain mg salts. -Hypermagnesemia can occur in a pt w/ untreated diabetic ketoacidosis when catabolism causes release of cellular mg that cannot be excreted b/c of profound fluid volume depletion & resulting oliguria. -Excess of mg can also result from excessive mg administered to treat hypertension of pregnancy or to treat low hypomagnesemia. -Increased serum mg lvls can also occur in adrenocortical insufficiency, Addison's disease, or hypothermia. -Excessive use of antacids (Maalox, Riopan, Mylanta); laxatives (Milk of Magnesia); and meds that decrease GI motility, including opioids & anticholinergics, can also increase serum mg lvls. -Decreased elimination of mg or its increased absorption due to intestinal hypomotility from any cause can contribute to hypermagnesemia. Lithium intoxication can cause an increase in serum mg lvls

Preparing to Administer IV Therapy: Using Ventipuncture Devices (Cannulas)

-Most peripheral access devices are cannulas. -General guidelines for selecting a cannula include: (1) Length: 0.75 to 1.25 inches long, (2) Diameter: Narrow diameter of the cannula to occupy min space within the vein, & (3) Gauge: 20 to 22 gauge for most IV fluids; larger gauge for caustic or viscous solutions; 14 to 18 gauge for blood administration & for trauma pts & those undergoing surgery. -Cannulas have an obturator inside a tube that is later removed. -Main types of cannula devices available are those referred to as winged infusion sets (butterfly) w/ a steel needle or as over-the-needle catheters w/ wings; indwelling plastic cannulas that are inserted over a steel needle; & indwelling plastic cannulas that are inserted through a steel needle. -Scalp vein or butterfly needles are short steel needles w/ plastic wing handles. Easy to insert, but b/c they are small & nonpliable, infiltration occurs easily. Use of these needles should be limited to obtaining blood specimens & not for IV meds b/c they increase risk of vein injury & infiltration. -Plastic cannulas inserted through a hollow needle are usually called intracatheters. Available in long lengths & are well suited for placement in central locations. B/c insertion requires threading cannula through the vein for a relatively long distance, these can be difficult to insert. -Most commonly used infusion device is the over-the-needle catheter. A hollow metal stylet is preinserted into the catheter & extends through the distal tip of the catheter to allow puncture of the vessel, in an effort to guide the catheter as the venipuncture is performed. The vein is punctured & a flashback of blood appears in the closed chamber behind the catheter hub. Once flashback has occurred, the catheter is threaded through the stylet into the vein & the stylet is then removed. -Many types of cannulas are available for IV therapy. Some of the variations in these cannulas include the thickness of the cannula wall (affects rate of flow), sharpness of the insertion needles (determines needle insertion technique), softening properties of the cannula (influences the length of time the cannula can remain in place), safety features (minimizes risk of needlestick injuries & bloodborne exposure), & the # of lumens (determines the # of solutions that can be infused simultaneously)

Isotonic Fluids: Normal Saline Solution

-Normal saline (0.9% sodium chloride) solution has a total osmolality of 308 mOsm/L. -B/c the osmolality is entirely contributed by electrolytes, the solution remains within the ECF. For this reason, NS solution is often used to correct an extracellular volume deficit. -NS contains only sodium & chloride & does not actually simulate the ECF. It is used w/ administration of blood transfusions & to replace large sodium losses, as in burn injuries. -It is not used for heart failure, pulmonary edema, renal impairment, or sodium retention. NS does not supply calories. -In pts w/ trauma or penetrating injury recent data has suggested maintaining a slightly hypotensive state until hemostasis has been achieved; therefore, the rapid administration of 0.9% NS is not ordered as often as it had been. -Hemorrhage can also begin a process of coagulopathy, acidosis, & hypothermia within the body, necessitating a decision for light vs. aggressive parenteral fluid administration

Hypophosphatemia: Nursing Management

-Nurse identifies pts who are at risk for hypophosphatemia & monitors them. -B/c malnourished pts receiving parenteral nutrition are at risk when calories are introduced too aggressively, preventive measures involve gradually introducing solution to avoid rapid shifts of phosphorus into the cells. -For pts w/ documented hypophosphatemia, careful attn is given to preventing infection, b/c hypophosphatemia may alter granulocytes. -In pts requiring correction of phosphorus losses, nurse freq monitors serum phosphorus lvls & documents & reports early signs of hypophosphatemia (apprehension, confusion, change in lvl of consciousness). -If pt experiences mild hypophosphatemia, foods such as milk & milk products, organ meats, nuts, fish, poultry, & whole grains should be encouraged. -W/ moderate hypophosphatemia, supplements such as Neutra-Phos capsules or Fleet's Phospho-Soda may be prescribed

Hypochloremia: Nursing Management

-Nurse monitors pt's I&O, ABG values, & serum electrolyte lvls, as well as lvl of consciousness & muscle strength & movement. Changes are reported to the provider promptly. -Vital signs are monitored, & resp assessment is carried out freq. Nurse teaches the pt about foods w/ high chloride content

Hyperphosphatemia: Nursing Management

-Nurse monitors pts at risk for hyperphosphatemia. -If a low-phosphorus diet is prescribed, the pt is instructed to avoid phosphorus-rich foods such as hard cheese, cream, nuts, meats, whole-grain cereals, dried fruits, dried vegetables, kidneys, sardines, sweetbreads, & foods made w/ milk. -When appropriate, nurse instructs the pt to avoid phosphate-containing substances such as lax & enemas. -Nurse also teaches pt to recognize the signs of impending hypocalcemia & to monitor for changes in urine output.

Types of IV Solutions: Hypotonic Fluids

-One purpose of hypotonic solutions is to replace cellular fluid. Another is to provide free water for excretion of body wastes. At times, hypotonic sodium solutions are used to treat hypernatremia & other hyperosmolar conditions. -Half-strength saline (0.45% sodium chloride) solution, w/ an osmolality of 154 mOsm/L, is freq used. Multiple-electrolyte solutions are also available. -Excessive infusions of hypotonic solutions can lead to intravascular fluid depletion by causing a fluid shift from blood vessels to cells, resulting in decreased BP, cellular edema, & cell damage. -These solutions exert less osmotic pressure than the ECF.

Phosphorous Imbalances

-Phosphorus is a critical constituent of all the body's tissues. It is essential to the function of muscle & RBC, the formation of adenosine triphosphate (ATP) & of 2,3-diphosphoglycerate, which facilitates release of oxygen from hemoglobin, & the maintenance of acid-base balance, as well as to the nervous system & the intermediary metabolism of carbohydrate, protein, & fat. -It provides structural support to bones & teeth in the form of phosphate. -Phosphorus is the primary anion of the ICF. About 85% of phosphorus is located in bones & teeth, 14% in soft tissue, & less than 1% in ECF. -Normal serum phosphorus lvl is 2.5 to 4.5 mg/dL.

Hypophosphatemia: Medical Management

-Prevention of hypophosphatemia is the goal. -In pts at risk for hypophosphatemia, serum phosphate lvls should be closely monitored & correction initiated before deficits become severe. -Adequate amounts of phosphorus should be added to parenteral solutions, & attn should be paid to phosphorus lvls in enteral feeding solutions. -Severe hypophosphatemia is dangerous & requires prompt attn. Aggressive IV phosphorus correction is usually limited to the pt whose serum phosphorus lvls decrease to less than 1 mg/dL & whose GI tract is not functioning. -Possible dangers of IV admin of phosphorus include tetany from hypocalcemia & calcifications in tissues (blood vessels, heart, lung, kidney, eyes) from hyperphosphatemia. -IV preparations of phosphorus are available as sodium or potassium phosphate. Rate of phosphorus admin should not exceed 10 mEq/h, & the site should be carefully monitored b/c tissue sloughing & necrosis can occur w/ infiltration. -In less acute situations, oral phosphorus replacement is usually adequate.

Hypermagnesemia: Nursing Management

-Pts at risk identified & assessed -Nurse monitors vital signs, noting hypotension & shallow respirations, or ECG abnormalities. -Nurse also observes for decreased deep tendon reflexes & changes in lvl of consciousness. -Meds that contain mg are not administered to pts w/ renal failure or compromised renal function, & pts w/ renal failure are cautioned to check w/ their health care providers before taking OTC meds. -Caution essential when preparing & administering magnesium-containing fluids parenterally, b/c available parenteral magnesium solutions (e.g., 2 mL ampules, 50 mL vials) differ in concentration.

Preparing to Administer IV Therapy: Using Ventipuncture Devices (Peripherally Inserted Central Cath or Peripheral-Midline Cath Access Line) (Table 4-7)

-Pts who need moderate- to long-term parenteral therapy often receive a peripherally inserted central cath (PICC or PIC line) or a peripheral-midline cath. -Also used for pts w/ limited peripheral access who require IV antibiotics, blood, vasopressors, or parenteral nutrition. -For these devices to be used, the median cephalic, basilic, & cephalic veins must be patent & undamaged. -Insertion of these caths are typically performed by specialized nurses who are trained in the use of them, as well as in the use of ultrasonography (used to visualize the vein to be canalized). -If these veins are damaged, then central venous access via subclavian or internal jugular vein, or surgical placement of an implanted port or vascular access device, must be considered as alternative. -Provider prescribes the line & the solution to be infused. -Insertion of either cath requires sterile technique. -Size of the cath lumen chosen is based on the type of solution, pt's body size, & vein to be used. Pt's consent is obtained before use of these caths. -Use of the dominant arm is recommended as the site for inserting the cannula into the superior vena cava to ensure adequate arm movement, which encourages blood flow & reduces risk of dependent edema or emboli formation. -Contraindications to arm choice include prior mastectomy, pacemaker placement, hemiparesis, & dialysis shunt.

Monitoring Flow: Discontinuing an Infusion

-Removal of an IV cath is associated w/ 2 possible dangers: bleeding & cath embolism. -To prevent excessive bleeding, a dry, sterile pressure dressing should be held over the site as the cath is removed. Firm pressure is applied until hemostasis occurs. -If a plastic IV cath is severed, the pt is at risk for cath embolism. To detect this complication when the cath is removed, the nurse compares expected length of the cath w/ its actual length. -Plastic caths should be withdrawn carefully & their length measured to make certain that no fragment has broken off in the vein. -Great care must be exercised when using scissors around dressing site. If the cath clearly has been severed, the nurse can attempt to occlude the vein above the site by applying a tourniquet to prevent the cath from entering the central circulation (until surgical removal is possible). -It is better to prevent a potentially fatal problem than to deal w/ it after it has occurred. Cath embolism can be prevented easily by following simple rules: (1) Avoid using scissors near cath, (2) Avoid withdrawing cath through the insertion needle, & (3) Follow manufacturer's guidelines carefully

Hyperchloremia: Clinical Manifestations and Assessment

-S/S of hyperchloremia are the same as those of metabolic acidosis, hypervolemia, & hypernatremia. -Tachypnea; weakness; lethargy; deep, rapid respirations; diminished cognitive ability; & hypertension occur. -If untreated, hyperchloremia can lead to a decrease in cardiac output, arrhythmias, & coma. -High chloride lvl is often accompanied by a high sodium lvl & fluid retention. -Lab analysis reveals serum chloride lvl is 108 mEq/L or greater, serum sodium lvl is greater than 145 mEq/L, serum pH is less than 7.35, & serum bicarbonate lvl is less than 22 mEq/L

Hypocalcemia: Nursing Management

-Seizure precaution initiated if hypocalcemia is severe. -Status of airway is closely monitored, b/c laryngeal stridor can occur. Tracheotomy tray should be kept at bedside, & manual resuscitation bag nearby, in case of laryngospasm in pts w/ audible stridor. -Safety precautions taken if confusion is present. -B/c of cardiac complications, ECG monitoring should be instituted to detect changes in heart rate & rhythm, esp if pt is receiving digoxin. -Ppl who have high risk for osteoporosis are instructed about the need for adequate dietary calcium intake; important to teach pt which foods are rich in calcium. -Nurse must also advise pt to consider calcium supplements if sufficient calcium is not consumed in the diet. Supplements should be taken in divided doses w/ meals. -In addition, the value of reg weight-bearing exercise in decreasing bone loss should be emphasized, as well as the effect of meds on calcium balance. -Additional teaching includes discussion of bisphosphonate meds to reduce the rate of bone loss. -Teaching also includes strategies to reduce risk of falls. -Patient is cautioned to avoid overuse of lax & antacids that contain phosphorus, b/c their use decreases calcium absorption.

Isotonic Fluids: Other Isotonic Solutions

-Several other solutions contain ions in addition to sodium & chloride & are somewhat similar to the ECF in composition. -Lactated Ringer's solution contains potassium & calcium in addition to sodium & chloride & can be used to correct dehydration & sodium depletion or to replace GI losses. Lactated Ringer's solution contains bicarbonate precursors as well. -Lactated Ringer's is typically not used in pts w/ severe acidosis or in advanced liver disease, which can affect lactate metabolism

Isotonic Fluids: D5W

-Solution of D5W has a serum osmolality of 252 mOsm/L. -Once administered, the glucose is rapidly metabolized, & this initially isotonic solution then disperses as a hypotonic fluid, one-third extracellular & two-thirds intracellular. Essential to consider this action of D5W, esp if the pt is at risk for increased intracranial pressure. -During fluid resuscitation, this solution should not be used, b/c of its limited ability to expand the intravascular volume. -D5W is used mainly to supply water & to correct an increased serum osmolality. About 1 L of D5W provides fewer than 200 kcal & is a minor source of the body's daily caloric requirements

Hypercalcemia: Clinical Manifestations and Assessment

-Symptoms of hypercalcemia are proportional to the degree of elevation of the serum calcium lvl. -Hypercalcemia reduces neuromuscular excitability b/c it suppresses activity at the myoneural junction. -Symptoms such as muscle weakness, incoordination, anorexia, & constipation may be caused by decreased tone in smooth & striated muscle. -Cardiovascular effects include hypertension & a shortened QT interval, which can cause increased sensitivity to digitalis & deposition of calcium in heart valves, myocardium, or coronary arteries. -Cardiac standstill can occur when the serum calcium level is about 18 mg/dL. -Anorexia, nausea, vomiting, & constipation are common symptoms of hypercalcemia. Abdominal & bone pain may also be present. Abdominal distention & paralytic ileus may complicate severe hypercalcemic crisis. -Excessive urination due to disturbed renal tubular function produced by hypercalcemia may occur. -Severe thirst secondary to polyuria caused by high solute (calcium) load is expected. -Although uncommon, pts w/ chronic hypercalcemia may develop symptoms similar to those of peptic ulcer b/c hypercalcemia increases secretion of acid & pepsin by the stomach. -Confusion, impaired memory, slurred speech, lethargy, acute psychotic behavior, or coma may occur. -The more severe symptoms tend to appear when the serum calcium level is approximately 16 mg/dL (4 mmol/L) or higher. However, some pts become profoundly disturbed w/ serum calcium levels of only 12 mg/dL. These symptoms resolve as serum calcium levels return to norm after treatment. -Hypercalcemic crisis refers to an acute rise in serum calcium lvl to 17 mg/dL or higher. Severe thirst and polyuria are often present. Other findings may include muscle weakness, intractable nausea, abdominal cramps, obstipation (very severe constipation) or diarrhea, peptic ulcer symptoms,& bone pain. Lethargy, confusion, & coma may also occur. Condition is very dangerous & may result in cardiac arrest. -Mnemonic "bones (bone pain), stones (kidney), groans (pain) & psychic moans (anxiety, psychiatric symptoms)" may be helpful to recall cascade of symptoms associated w/ hypercalcemia. -Serum calcium lvl is greater than 10.2 mg/dL. -Double-antibody PTH test may be used to differentiate b/w primary hyperparathyroidism & malignancy as a cause of hypercalcemia: PTH levels are increased in primary or secondary hyperparathyroidism & suppressed in malignancy. -X-rays may reveal presence of osteoporosis if the pt has hypercalcemia secondary to a malignancy or bone cavitation. -24-hr urine calcium collection may be ordered; hypercalciuria is defined as calcium excretion of greater than 400 mg/day.

Managing Systemic Complications

-Systemic complications occur less freq but are usually more serious than local complications. They include circulatory overload, air embolism, febrile reaction, & infection. -Overloading the circulatory system w/ excessive IV fluids causes increased BP & central venous pressure. S/S of fluid overload include moist crackles on auscultation of lungs, edema, weight gain, dyspnea, & respirations that are shallow/ have an increased rate. -Possible causes include rapid infusion of an IV solution or hepatic, cardiac, or renal disease. Risk of fluid overload & subsequent pulmonary edema is esp increased in elderly pts w/ cardiac disease; this is referred to as circulatory overload. -Treatment for circulatory overload is decreasing the IV rate, monitoring vital signs freq, assessing breath sounds, & placing pt in a high Fowler's position. Provider is contacted immediately. -This complication can be avoided by using an infusion pump for infusions & by carefully monitoring all infusions. -Complications of circulatory overload include heart failure & pulmonary edema. -Risk of air embolism is rare but ever-present. Most often associated w/ cannulation of central veins. Manifestations of air embolism include dyspnea & cyanosis; hypotension; weak, rapid pulse; loss of consciousness; & chest, shoulder, & low back pain. -Treatment calls for immediately clamping the cannula & replacing a leaking or open infusion system, placing the pt on the left side in Trendelenburg position, assessing vital signs & breath sounds, & administering oxygen. -Air embolism can be prevented by using a Luer-Lock adapter on all lines, filling all tubing completely w/ solution, & using an air detection alarm on an IV pump. -Complications of air embolism include shock & death. Amount of air necessary to induce death in humans is not known; however, rate of entry is probably as important as the actual volume of air. -Pyrogenic substances in either the infusion solution or the IV administration set can induce a febrile reaction & septicemia. -S/S include an abrupt temperature elevation shortly after infusion is started, backache, headache, increased pulse & resp rate, nausea & vomiting, diarrhea, chills & shaking, & general malaise. -In severe septicemia, vascular collapse & septic shock may occur. Causes of septicemia include contamination of the IV product or a break in aseptic technique, esp in immunocompromised pts. -Treatment is symptomatic & includes culturing of the IV cannula, tubing, or solution if it is suspect, & establishing a new IV site for med or fluid administration. -Infection ranges in severity from local involvement of the insertion site to systemic dissemination of organisms through the bloodstream, as in septicemia. -Measures to prevent infection are essential at the time the IV line is inserted & throughout the entire infusion.

Nursing Management of the Patient Receiving IV Therapy

-The ability to perform venipuncture to gain access to the venous system for administering fluids & med is an expected nursing skill in many settings. -This responsibility includes selecting appropriate venipuncture site & type of cannula & being proficient in the technique of vein entry. -This skill should be mastered by all bedside nurses, & it is up to each individual nurse to seek out the opportunity to learn & practice venipuncture

Preparing to Administer IV Therapy: Using Ventipuncture Devices (Needleless IV Delivery Systems)

-The federal Needlestick Safety & Prevention Act (signed into law in November 2000) requires needleless systems in an effort to decrease needlestick injuries & exposure to HIV, hepatitis, & other bloodborne pathogens. -These systems have built-in protection against needlestick injuries & provide a safe means of using & disposing of an IV administration set (which consists of tubing, an area for inserting the tubing into the container of IV fluid, and an adapter for connecting the tubing to the needle). -IV line connectors allow the simultaneous infusion of IV meds & other intermittent meds (piggyback delivery) w/o the use of needles. -Technology is advancing & moving away from use of the traditional stylet. Many examples of these devices are on the market.

Hypercalcemia: Medical Management

-Therapeutic aims include decreasing serum calcium lvl & reversing the process causing hypercalcemia. -General measures include administering fluids to dilute serum calcium & promote its excretion by the kidneys, mobilizing the pt, & restricting intake of fluids & meds that contain calcium. -IV admin of 0.9% sodium chloride solution is expected since it temporarily dilutes serum calcium lvl & increases urinary calcium excretion by inhibiting tubular reabsorption of calcium. -Furosemide (Lasix) is often used in conjunction w/ administration of a saline solution; in addition to causing diuresis, furosemide increases calcium excretion & is useful in preventing fluid volume excess associated w/ saline administration. -Calcitonin can be used to lower serum calcium lvl & is particularly useful for pts w/ heart disease or renal failure who cannot tolerate large sodium loads. Calcitonin reduces bone resorption, increases the depositing of calcium & phosphorus in the bones, and increases urinary excretion of calcium & phosphate. -Although several forms available, calcitonin derived from salmon is commonly used. Skin testing for allergy to salmon calcitonin is necessary before hormone is administered. -Systemic allergic reactions are possible because this hormone is a protein; resistance to the med may develop later b/c of antibody formation. -Calcitonin is administered by IM injection rather than subq, b/c pts w/ hypercalcemia have poor perfusion of subq tissue. -For pts w/ cancer, treatment is directed at controlling condition by surgery, chemotherapy, or radiation therapy. -Corticosteroids may be used to decrease bone turnover & tubular reabsorption for pts w/ sarcoidosis, myelomas, lymphomas, & leukemias; pts w/ solid tumors are less responsive. -Bisphosphonates inhibit osteoclast activity & may be used to lower serum calcium lvls. -Mithramycin, a cytotoxic antibiotic, inhibits bone resorption & thus lowers serum calcium lvl. This agent must be used cautiously b/c it has significant side effects, including thrombocytopenia, nephrotoxicity, rebound hypercalcemia when discontinued, & hepatotoxicity. -Inorganic phosphate salts can be administered orally or by NG tube (in the form of Phospho-Soda or Neutra-Phos), rectally, or intravenously. -IV phosphate therapy is used w/ extreme caution in treatment of hypercalcemia, b/c it can cause severe tissue calcification, hypotension, tetany, & acute renal failure. Typically, IV phosphate reserved for hypercalcemia that is unresponsive to other agents. -Hemodialysis or peritoneal dialysis w/ low calcium lvls in dialysis fluid may be considered since both treatments are effective for removing calcium from circulation. Dialysis may be considered for pts w/ renal insufficiency & congestive heart failure in which saline infusion is not suitable

Hypochloremia: Medical Management

-Treatment involves correcting the cause of hypochloremia & the contributing electrolyte & acid-base imbalances. -Normal saline (0.9% sodium chloride) or half-strength saline (0.45% sodium chloride) solution is administered by IV to replace chloride. -Provider may reevaluate whether pt receiving a diuretic (loop, osmotic, or thiazide) should discontinue the meds or change to another diuretic. -Foods high in chloride are provided; includes tomato juice, bananas, dates, eggs, cheese, milk, salty broth, canned vegetables, & processed meats. -Pt who drinks free water (water w/o electrolytes) or bottled water excretes large amounts of chloride; therefore, pt instructed to avoid this kind of water. -Ammonium chloride, an acidifying agent, may be prescribed to treat metabolic alkalosis; dosage depends on pt's weight & serum chloride lvl. This agent is metabolized by the liver, & its effects last for about 3 days. Its use should be avoided in pts w/ impaired liver or renal function

Hyperphosphatemia (Phosphorous Excess)

-Various conditions can lead to this imbalance, but most common is renal failure. -Other causes include increased intake, decreased output, or a shift from the intracellular to extracellular space. -Other causes include chemotherapy for neoplastic disease, hypoparathyroidism, metabolic or respiratory acidosis, diabetic ketoacidosis, acute hemolysis, high phosphate intake, profound muscle necrosis, & increased phosphorus absorption. -Primary complication of increased phosphorus is metastatic calcification (soft tissue, joints, and arteries), which occurs when the calcium-magnesium product (calcium × magnesium) exceeds 70 mg/dL

Preparing to Administer IV Therapy: Choosing an IV Site

-Veins of the extremities are designated as peripheral locations & are ordinarily the only sites used by nurses. -B/c they are relatively safe & easy to enter, arm veins are most commonly used. The metacarpal, cephalic, basilic, & median veins & their branches are recommended sites b/c of their size & ease of access. -More distal sites should be used first, w/ more proximal sites used subsequently. -Leg veins should rarely, if ever, be used b/c of high risk of thromboembolism. -Additional sites to avoid include veins distal to a previous IV infiltration or phlebitic area, sclerosed or thrombosed veins, an arm w/ an arteriovenous shunt or fistula, & an arm affected by edema, infection, blood clot, or skin breakdown. -Central veins commonly used by physicians & trained health providers include the subclavian & internal jugular veins. It is possible to gain access to (or cannulate) these larger vessels even when peripheral sites have collapsed, & they allow for the admin of hyperosmolar solutions & vasoconstrictive drugs. Potential hazards are much greater & include inadvertent entry into an artery or the pleural space, as well as a higher risk of infection. -Both arms & hands are carefully inspected before a specific venipuncture site that does not interfere w/ mobility is chosen. For this reason, antecubital fossa is avoided, except as a last resort. -Most distal site of the arm or hand is generally used first, so that subsequent IV access sites can be moved progressively upward. -Factors should be considered when selecting a site for venipuncture: (1) Condition of vein, (2) Type of fluid or med to be infused, (3) Duration of therapy, (4) Pt's age & size, (5) Whether pt is right- or left-handed (6) Pt's medical history & current health status, & (7) Skill of the person performing the venipuncture. -After applying a tourniquet, nurse palpates & inspects the vein. Tourniquet remains applied for a max of 3 mins before tension must be released. -The vein should feel firm, elastic, engorged, & round—not hard, flat, or bumpy. -B/c arteries lie close to veins in the antecubital fossa, the vessel should be palpated for arterial pulsation (even with a tourniquet on), & cannulation of pulsating vessels should be avoided

Types of IV Solutions: Hypertonic Fluids

-When NS solution or lactated Ringer's solution contains 5% dextrose, the total osmolality exceeds that of the ECF. However, the dextrose is quickly metabolized, & only the isotonic solution remains. Therefore, any effect on the intracellular compartment is temporary. -Higher concentrations of dextrose, such as 50% dextrose in water, are administered to help meet caloric requirements. These solutions are strongly hypertonic & must be administered into central veins, so that they can be diluted by rapid blood flow. -Saline solutions are also available in osmolar concentrations greater than that of the ECF. These solutions draw water from the ICF to the ECF & cause cells to shrink. -If administered rapidly or in large quantity, they may cause an extracellular volume excess & precipitate circulatory overload. As a result, these solutions must be administered cautiously & usually only when the serum osmolality has decreased to dangerously low levels. -Hypertonic solutions exert an osmotic pressure greater than that of the ECF.

Parental Fluid Therapy

-When no other route of administration is available, fluids are administered intravenously in hospitals, outpatient diagnostic & surgical settings, clinics, & homes to replace fluids, administer meds, & provide nutrients. -Typical indications for giving a fluid bolus include hypotension, low urine output, & inadequate cardiac output for tissue needs

Hyperphosphatemia: Medical Management

-When possible, treatment is directed at the underlying disorder. -In renal failure, elevated PTH production contributes to a high phosphorus lvl & bone disease. -Measures to decrease serum phosphate lvl in these pts include vit D preparations, such as calcitriol, available in both oral (Rocaltrol) and parenteral (Calcijex, paricalcitol) forms. IV admin of calcitriol does not increase serum calcium unless its dose is excessive, thus permitting more aggressive treatment of hyperphosphatemia w/ calcium-binding antacids (calcium carbonate or calcium citrate), phosphate-binding gels or antacids, restriction of dietary phosphate, forced diuresis w/ a loop diuretic, volume repletion w/ saline, & dialysis. -Surgery may be indicated for removal of large calcium-phosphorus deposits

Types of IV Solutions: Other IV Substances

-When the pt's GI tract is unable to tolerate food, nutritional requirements are often met using the IV route. -Parenteral solutions may include high concentrations of glucose, protein, or fat to meet nutritional requirements. Parenteral route may also be used to administer colloids, plasma expanders, & blood products including packed RBC, fresh frozen plasma, & platelets. -Many meds are also delivered by the IV route, either by infusion or directly into the vein. -While all meds may produce reactions IV meds are esp dangerous due to the rapid introduction & absorption within the bloodstream. -Astute nursing includes knowledge of the administration rates & recommended dilutions for any med given

Hypophosphatemia: Clinical Manifestations and Assessment

-Wide range of neuro symptoms, such as irritability, fatigue, apprehension, weakness, numbness, paresthesias, dysarthria, dysphagia, diplopia, confusion, seizures, & coma, may occur. -Low lvls of diphosphoglycerate may reduce the delivery of oxygen to peripheral tissues, resulting in tissue anoxia. Hypoxia then leads to an increase in resp rate & resp alkalosis, causing phosphorus to move into the cells & potentiating hypophosphatemia. -It is thought that hypophosphatemia may predispose a person to infection due to a decrease in granulocyte function. Muscle damage may develop as the ATP lvl in muscle tissue declines. -Clinical manifestations are muscle weakness, may be subtle or profound & may affect any muscle group, muscle pain, & at times acute rhabdomyolysis (disintegration of striated muscle). Weakness of resp muscles may greatly impair ventilation. -Hypophosphatemia may predispose a person to insulin resistance & thus hyperglycemia. -Chronic loss of phosphorus can cause bruising & bleeding from platelet dysfunction. -On lab analysis, serum phosphorus lvl is less than 2.5 mg/dL. When reviewing lab results, nurse should keep in mind that glucose or insulin admin causes a slight decrease in serum phosphorus lvl. -If hypophosphatemia is associated w/ hyperparathyroidism, serum PTH lvls are increased. -If etiology of hypophosphatemia is related to increased osteoblastic activity serum alkaline, phosphatase is increased. X-rays may show skeletal changes of osteomalacia or rickets

Normal Values for Arterial Blood Gasses

-pH 7.35-7.45 -PaCO2 35-45 mm Hg -PaO2 80-100 mm Hg -HCO3 22-26 mEq/L

Hypocalcemia (Calcium Deficit)

Hypocalcemia (lower-than-normal serum concentration of calcium), or less than 8.2 mg/dL & ionized calcium of less than 4.6 mg/dL, occurs in a variety of clinical situations

Hypercalcemia (Calcium Excess)

Hypercalcemia (excess of calcium in the plasma) is a dangerous imbalance. Hypercalcemic crisis (acute increase in calcium level) has an extremely high mortality rate if not corrected promptly, often related to cardiac arrest