Chapter 42 (3101)

Chapter 42: Fluids and Electrolytes Fluid surrounds all the cells in the body and is also inside cells. Body fluids contain electrolytes such as sodium and potassium; they also have a certain degree of acidity. Fluid, electrolyte, and acid-base balances within the body maintain the health and function of all body systems. Location and Movement of Water/Electrolytes  Water: 60% body weight; decreases with age. Fluid Distribution  ECF: outside cells; ICF: inside cells.  ICF: 2/3 of total body water; ECF: 1/3 of total body water  ECF: Intravascular(liquid part in blood) and interstitial fluid (between cells and outside blood vessels). Transcellular: cerebrospinal, pleural, peritoneal, and synovial fluids. Composition of Body Fluids  Electrolyte: compound that separates into ions when it dissolves in water. o Cations (pos): NA, K, Ca, Mg. o Anions (neg): Cl, Bicarb.  Osmolality: measure of number of particles per kilogram of water o Tonicity: effective concentration o Isotonic: same as blood o Hypotonic: more dilute than blood o Hypertonic: more concentrated than blood  Active Transport: requires energy in form of ATP to move electrolytes across membrane against concentration gradient (low to high). o Example: Sodium Potassium Pump: moves Na out of cell and K into it, keeping ICF lower in Na and higher in K than ECF.  Diffusion: passive movement of electrolytes or other particles down a concentration gradient (high to low). Diffuse easily by random movements until concentrations is same in all areas. o Require proteins that serve as ion channels. Opening of ion channels: tightly controlled and plays part in muscle and nerve function.  Osmosis: water moves through membrane that separates fluids with different particle concentrations. o Osmotic Pressure: inward pulling force caused by particles in fluid; particles already inside cell exert ICF pressure. Pull water into cell; particles in interstitial fluid exert interstitial fluid osmotic pressure and pull water out of cell.  Filtration: net effect of four forces, two tend to move fluid out of capillaries and small venules and two tend to move fluid back into them. o Hydrostatic Pressure: force of fluid pressing outward against surface.  Colloids: albumin and other proteins in blood o Much larger than electrolytes, glucose, and molecules. o Too large to leave capillaries in fluid that is filtered

o Exert osmotic pressure: Oncotic Pressure: inward pulling force caused by blood proteins that help move fluid from interstitial area back into capillaries. o Capillary Hydrostatic Pressure: strongest at arterial end; fluid moves from capillary into interstitial area, bringing nutrients into cell. Venous end: CHP is weaker and OP is stronger. Fluid moves into venous end capillary, removing wastes. BUN (Blood Urea Nitrogen)  BUN: indicates renal function and hydration status  Normal Range: 10-20mg/dL (slightly higher in older patients); Critical Value: >100mg/dL  Increased BUN: dehydration, excessive protein intake and impaired renal function.  Decreased DUN: overhydration, liver damage, and malnutrition. Hydration  Specific Gravity, Hematocrit (Hct), and Sodium. o Go Up: Fluid Volume Deficit-Dehydration o Go Down: Fluid Volume Excess- Overhydration  Normal Hct: 3 x Hemoglobin (Hgb) (37% Hct)  Hemodilution: 12gm Hgb (27% Hct)  Hemoconcentration: 12gm Hgb (47% Hct) Fluid Balance  Isotonic: no change  Hypotonic: Cell swells  Hypertonic: Cell shrinks Top 5 Fluids  NS 0.9% (NaCl): used to expand volume, dilute medications, and keep veins open.  Lactated Ringer: Fluid resuscitation o NS and LR are ISOTONIC: same osmolarity as body fluid  D5W: HYPOTONIC (iso until inside body-metabolize glucose-become hypo) o DO NOT: give to infants or head injury patients: Causes cerebral edema.  D5 ½ NS (D5NS): Sodium and volume replacement: HYPERTONIC o Go slow! Monitor BP, pulse, quality of lung sounds, and urine output. Fluid Balance  Maintain fluid balance: fluid intake = fluid output. o Normal daily fluid output (e.g., urine, sweat) is a hypotonic salt solution, people must have equal fluid intake of hypotonic sodium-containing fluid (or water plus foods with some salt) to maintain fluid balance.  Fluid Intake: Orally through drinking and eating (most foods contain some water) o Food metabolism creates additional water. o Average fluid intake: 2300 mL o Other routes of fluid intake: intravenous (IV), rectal (e.g., enemas), and irrigation of body cavities that can absorb fluid.  Fluid Distribution: movement of fluid among its various compartments.

o Atrial Natriuretic Peptide: regulates ECV by influencing how much sodium and water are excreted in urine.  Cells in the atria of the heart release ANP when they are stretched (e.g., by an increased ECV).  ANP: weak hormone that inhibits ADH by increasing the loss of sodium and water in the urine (see Fig. 42-6, C).  ANP opposes the effect of aldosterone. Thirst  Important regulator of fluid intake when plasma osmolality increase; conscious desire for water.  Thirst control is located in hypothalamus.  Thirst-Control Mechanism o Increase plasma osmolality: osmoreceptor-mediated thirst. o Angiotensin II: baroreceptor-mediated thirst and angiotensin II o Angiotensin III: baroreceptor-mediated thirst and angiotensin III o Dry pharyngeal mucous membranes o Decreased plasma volume o Psychological factors Imbalance and Related Causes Signs and Symptoms Isotonic Imbalances: water and sodium loss of gained in equal or isotonic proportions. Extracellular FVD: body fluids have decreased volume but normal osmolality  Sodium and water intake less than output, causing isotonic loss.  Severely decreased oral intake of water and salt.  Increase GI output: vomit, diarrhea, laxatives, overuse, of drainage.  Increased renal output: diuretics, adrenal insufficiency.  Loss of blood of plasma: burns or hemorrhage.  Massive sweating without intake.  Sudden weight loss, postural hypotension, tachycardia, thready pulse, dry mucous membranes, poor skin turgor, slow vein filling, and dark urine.  Severe: thirst, restlessness, confusion, oliguria, cold skin, and hypovolemic shock.  Labs: increase Hct, Increased BUM, and Increased specific gravity. Extracellular FVE: body fluids have increased volume but normal osmolality  Sodium and water intake greater than output, causing isotonic gain.  Excessive admin of Na.  Renal retention of Na and water: heart failure, cirrhosis, aldosterone excess, or renal disease.  Sudden weight gain, edema, crackles in lungs.  Severe: confusion, and pulmonary edema.  Labs: decreased Hct, BUN, and gravity. Osmolality Imbalances Hypernatremia: Water Deficit: Body Fluids Too Concentrated  Loss of more water than salt  Diabetes (ADH deficit)  Large perspiration and respiratory water output without intake  Gain of more salt than water  Admin of tube feedings, TPN, lack of access to water, and dysfunction of  Decreased level of consciousness, thirsts, seizures  Labs: increased Na levels and osmolality.

osmoreceptor driven thirst drive. Hyponatremia: Water Excess: Fluids too Dilute  Gain of more water than salt: excessive ADH, excessive water intake, excessive IV admin, enemas.  Loss of more salt than water: replacement of large output (diarrhea and vomit).  Decreased level of consciousness, seizures.  Labs: decreased Na and osmolality levels. Combines Volume and Osmolality Imbalance Clinical Dehydration (ECV Deficit + Hypernatremia): Body Fluids Have Decreased Volume and Are Too Concentrated  Sodium and Water Intake Less than Output, with Loss of More Wate than Salt: poor water intake and ECV deficit.  ECV plus hypernatremia. Fluid Imbalances  Anything disrupts fluid intake/output (disease, meds, factors): imbalances. o Example: diarrhea: fluid output is increased; fluid imbalance (dehydration) occurs if fluid intake does not increase.  Two major types of fluid imbalances: Volume Imbalances and Osmolality Imbalances. o Volume imbalances: disturbances of the amount of fluid in the extracellular compartment. o Osmolality imbalances: disturbances of the concentration of body fluids.  Volume Imbalances o Extracellular fluid volume (ECV) imbalance: too little (ECV deficit) or too much (ECV excess) isotonic fluid is present.  ECV deficit and excess are abnormal volumes of isotonic fluid (sudden changes in body weight and changes in markers of vascular and interstitial volume).  ECV deficit is present: isotonic fluid is insufficient in the extracellular compartment.  ECV deficit: output of isotonic fluid exceeds intake of sodium-containing fluid (ECF is both vascular and interstitial); signs and symptoms arise from lack of volume.  ECV excess: too much isotonic fluid is found in the extracellular compartment.  Intake of sodium-containing isotonic fluid has exceeded fluid output.  Eat more salty foods: ankles swell or rings on your fingers feel tight and weight gain.  Osmolality Imbalances o Body fluids become hypertonic or hypotonic: osmotic shifts of water across cell membranes. o Osmolality imbalances: hypernatremia and hyponatremia.  Hypernatremia (water deficit): hypertonic condition.  Loss of relatively more water than salt, or gain of relatively more salt than water.  Interstitial fluid becomes hypertonic: water leaves cells by osmosis, and they shrivel.  SS: cerebral dysfunction, which arise when brain cells shrivel.  Hyponatremia (water excess): hypotonic condition.

 Distribution: plasma concentrations (K, Ca, Mg, Ph) very low compared with cell/bone concentrations.  Output: urine, feces, sweat, vomiting, drainage, and fistulas.  Potassium (K) o Hypokalemia: low K concentration in blood  Results from: decreased potassium intake and absorption, a shift of potassium from the ECF into cells, and an increased potassium output.  Common causes: increased potassium output, diarrhea, repeated vomiting, and use of potassium-wasting diuretics.  SS: muscle weakness, respiratory muscles and potentially life-threatening cardiac dysrhythmias. Hyporeflexia, alkalosis, shallow breaths, irritability, confusion, tachycardia, lethargy, thready pulse, and decrease intestinal motility.  EKG: Flat T wave; ST depression. o Hyperkalemia: high K concentration in blood  Causes: increased potassium intake and absorption, shift of potassium from cells into the ECF, and decreased potassium output. Rapid infusion of stored blood. DKA, oliguria, potassium sparing diuretics, and adrenal deficit.  People who have oliguria (decreased urine output) are at high risk of  SS: muscle weakness, potentially life-threatening cardiac dysrhythmias, and cardiac arrest. Irritability, diarrhea, EKG changes, twitches, cramps, low BP, decreased urine output, and cramps.  EKG: peak T wave, wide QRS, and long PR.  Calcium (Ca) o Hypocalcemia: Low Ca concentration in body  Causes: decreased Ca intake, shift of Ca into bone, or increased Ca output. Too much ionized calcium to shift to bound forms cause symptomatic ionized hypocalcemia. Hypoparathyroidism.  People who have acute pancreatitis frequently develop hypocalcemia because calcium binds to undigested fat in their feces and is excreted.  This process decreases absorption of dietary calcium and increases calcium output by preventing resorption of calcium contained in GI fluids.  SS: increases neuromuscular excitability, numbness and tingling, hyperreflexia. o Hypercalcemia: high Ca concentration in blood  Results from: increased calcium intake and absorption, shift of calcium from bones into the ECF, and decreased calcium output. Hyperparathyroidism  Patients with cancer often develop hypercalcemia because some cancer cells secrete chemicals into the blood that are related to parathyroid hormone.  SS: weak bones, pathological fractures, decreases neuromuscular excitability, and lethargy. Nausea, vomit, constipation, fatigue, hyporeflexia, decreased LOC.  Magnesium (Mg) o Hypomagnesemia: low Mg concentration in blood  Causes: decreased magnesium intake and absorption, shift of plasma magnesium to its inactive bound form, and increased magnesium output. Malnutrition, alcoholism, laxatives.  SS: increases neuromuscular excitability. Muscle cramps, twitching, tetany, seizures, insomnia, tachycardia, and hypertension. o Hypermagnesemia: high Mg concentration in blood

 End-stage renal disease causes hypermagnesemia unless the person decreases magnesium intake to match the decreased output.  SS: decreased neuromuscular excitability, with lethargy and decreased deep tendon reflexes. Acid Base Balance  Acid production, buffering, and excretion interplay to create balance. o Excretion: Lungs and Kindeys  Lungs excrete carbonic acid (exhale)  PaCO2 rises: chemoreceptors trigger faster and deeper respirations to excrete the excess.  PaCO2 falls,: chemoreceptors trigger slower and shallower respirations, so more of the CO2 produced by cells remains in the blood and makes up the deficit.  Kidneys excrete metabolic acid  Secrete H+ into the renal tubular fluid, putting HCO3− back into the blood at the same time.  Too many H+ ions are present in the blood: renal cells move more H+ ions into the renal tubules for excretion, retaining more HCO3− in the process.  Too few H+ ions are present in the blood: renal cells secrete fewer H+ ions.  Phosphate buffers in the renal tubular fluid keep the urine from becoming too acidic when the kidneys excrete H+ ions.  Kidneys need to excrete a lot of H+: renal tubular cells secrete ammonia, which combines with H+ ions in the tubules to make NH4+, ammonium ions.  Acids release hydrogen ions; bases (alkaline) take up hydrogen ions  Degree of acidity is Ph o 1: very acidic; 14: very basic (7: neutral) o Arterial Blood: 7.35-7.45  Laboratory tests: arterial blood called arterial blood gases (ABGs) used to monitor a patient’s acid-base balance  Buffers: pairs of chemicals that work to maintain normal pH of body fluids.  Buffering: Too many free H+ ions are present, a buffer takes them up, no longer are free. Too few are present, a buffer can release H+ ions to prevent an acid-base imbalance. o Major buffer in ECF: bicarbonate (HCO3−) buffer system, which buffers metabolic acids. o Too few H+ ions are present, the carbonic acid portion of the buffer pair will release some, increasing the bicarbonate, again returning pH to normal. o Buffers: hemoglobin, protein buffers, phosphate buffers, cellular and bone buffers. o Buffers normally keep the blood from becoming too acid when acids that are produced by cells circulate to the lungs and kidneys for excretion.  Alkalosis: Kicking up pH (+7.4)  Acidosis: Sliding Down pH (-7.1) Acid Base Imbalances

o Cause: decreases respiratory stimuli (anesthesia, drug overdose), COPD, pneumonia, and atelectasis. o SS: hypoventilation, hypoxia, rapid/shallow breaths, low BP with vasodilation, dyspnea, headache, hyperkalemia, dysrhythmias, drowsiness, dizziness, disorientation, muscle weakness, hyperreflexia.  Metabolic Acidosis: arises from increase in metabolic acid or decrease in base (bicarbonate) (problem: only kidneys can correct, lungs can compensate by changing amount of carbonic acid in blood) o Kidneys unable to excrete enough metabolic acids (accumulate in blood) o Decreased level of consciousness o Stimulates the chemoreceptors: respiratory system compensates for the acidosis by hyperventilation (process does not correct the problem, but it helps limit the pH decrease). o Causes: DKA, diarrhea, renal failure, or shock o SS: headache, decreased BP, hyperkalemia, muscle twitching, warm/flushed skin, nausea, vomiting, diarrhea, confusion, and Kussmaul respirations. Types of Alkalosis  Respiratory Alkalosis: arises from alveolar hypoventilation o Lungs excrete too much CO2 o Deficit from carbonic acid in blood increased pH o pH increases: cell membrane excitability increases (rise to neurological symptoms such as excitement, confusion, and paresthesia): central nervous system (CNS) depression. o Causes: hyperventilation (anxiety, exercise, fear) or mechanical ventilation o SS: seizures, deep/rapid breaths, tachycardia, low BP, hypokalemia, numbness or tingling extremities, lethargy, light headedness, nausea, and vomiting.  Metabolic Alkalosis: arises from direct increase in base (bicarbonate) or decrease in metabolic acid o Increase blood bicarbonate o Causes: vomiting and gastric suction, diuretics, and excessive NaHCO3. o Respiratory compensation for metabolic alkalosis is hypoventilation (decreased rate and depth of respiration allow carbonic acid to increase in the blood). o SS: hypoventilation, tachycardia, restlessness, lethargy, confusion, dizzy, irritable, nausea, vomiting, tremors, muscle cramps, and tingling.

Arterial Blood Gases Lab Measure Normal Range Definition pH 7.35-7.45 Negative logarithm of free hydrogen concentration, measure of blood’s acidity or alkalinity. Small changes in pH denote large changes in H+ concentration and are clinically important. PaCO2 35-45 Partial pressure of carbon dioxide (CO2), a measure of how well the lungs are excreting CO2 produced by cells. HCO3 21/28 HCO3− is concentration of the base (alkaline substance) bicarbonate, a measure of how well the kidneys are excreting metabolic acids. Increased HCO3− indicates that the blood has too few metabolic acids; decreased HCO3− indicates that the blood has too many metabolic acids. PaO2 80-100 PaO2 is partial pressure of oxygen (O2), a measure of how well gas exchange is occurring in the alveoli of the lungs. Values below normal indicate poor oxygenation of the blood. SaO2 95%-100% SaO2 is oxygen saturation, the percentage of hemoglobin that is carrying as much O2 as possible. It is influenced by pH, PaCO2, and body temperature. Base Excess -2-+2 observed buffering capacity minus the normal buffering capacity, a measure of how well the blood buffers are managing metabolic acids. Values below −2 (negative base excess) indicate excessive metabolic acids; values above +2 indicate excessive amounts of bicarbonate. Assessment  History o Age: very young (ECV deficit, dehydration), very old (ECV excess) o Environment: Na rich diet (ECV excess); hot weather (dehydration). o GI Output: Diarrhea (ECV deficit/dehydration); Drainage (ECV deficit); Vomit (ECV deficit).

 CO2: 22-28  BUN: 7-24  Cr: 0.7-1.4  Glu: 60-120  Ca: 9-11  Mg: 1.5-2.5  Phos: 3.5-4.5  Hgb: 10-16  Hct: 30-50 Kayexalate (Sodium Polystyrene Sulfonate)  PO or enema  Removes Potassium  Watch heart rhythm and Na  Causes: constipation, gastric irritation, diarrhea, and Na retention. Implementation  Enteral replacement of fluids, restriction of fluids, parenteral replacement (TPN, crystalloids, and colloids). IV Therapy: crystalloids  Goal: correct or prevent fluid and electrolyte disturbances. IVs allow direct access to the vascular system, permitting continuous infusion of fluids over a period of time.  Isotonic, hypotonic, and hypertonic  Too rapid or excess infusion: cardiac issues (NO IV PUSH)  Vascular access devices (VADs): catheters or infusion ports designed for repeated access to the vascular system. Peripheral catheters are for short-term use. o Devices for long-term use include central catheters and implanted ports, which empty into a central vein. o Peripherally inserted central catheters (PICC lines) enter a peripheral arm vein and extend through the venous system to the superior vena cava, where they terminate. o Central lines enter a central vein such as the subclavian or jugular vein or are tunneled through subcutaneous tissue before entering a central vein (more effective than peripheral catheters for administering large volumes of fluid, parenteral nutrition (PN), and medications or fluids that irritate veins).  Electronic infusion devices (EIDs), also called IV pumps or infusion pumps, deliver an accurate hourly IV infusion rate. EIDs use positive pressure to deliver a measured amount of fluid during a specified unit of time  Involves (1) keeping the system sterile and intact; (2) changing IV fluid containers, tubing, and contaminated site dressings; (3) assisting a patient with self-care activities so as not to disrupt the system; and (4) monitoring for complications of IV therapy.  Protective devices designed to prevent movement or accidental dislodgment of a VAD are called catheter stabilization devices.  Movement of the VAD in a vein can cause phlebitis and infiltration. o Infiltration: IV catheter becomes dislodged or a vein ruptures and IV fluids inadvertently enter subcutaneous tissue around the venipuncture site.

o Phlebitis: (inflammation of a vein) results from chemical, mechanical, or bacterial causes. Phlebitis can be dangerous because blood clots (thrombophlebitis) form along the vein and in some cases cause emboli. This may cause permanent damage to veins  Circulatory overload with IV solution: patient receives too-rapid administration or an excessive amount of fluids.  Older Adults: use smallest gauge, avoid back of hand. Avoid in veins that are easily bumped, avoid vigorous friction, use minimal pressure, place tourniquet over sleeve, lower insertion angle, stabilize vein, and medications increased bruising and bleeding.  To remove a gown, remove the sleeve of the gown from the arm without the IV line, maintaining the patient’s privacy. Remove the sleeve of the gown from the arm with the IV line. Remove the IV solution container from its stand and pass it and the tubing through the sleeve. (If this involves removing the tubing from an EID, use the roller clamp to slow the infusion to prevent the accidental infusion of a large volume of solution or medication.)  To apply a gown, place the IV solution container and tubing through the sleeve of the clean gown and hang it on its stand. (If the IV line is controlled by an EID, reassemble, turn on the pump, and open the roller clamp.) Place the arm with the IV line through the gown sleeve. Place the arm without the IV line through the other gown sleeve. Blood Transfusion  Blood component therapy = IV administration of whole blood  Objectives : (1) increasing circulating blood volume after surgery, trauma, or hemorrhage; (2) increasing the number of RBCs and maintaining hemoglobin levels in patients with severe anemia; and (3) providing selected cellular components as replacement therapy (e.g., clotting factors, platelets, albumin).  Blood transfusions must be matched to each patient to avoid incompatibility. o RBCs have antigens in their membranes; the plasma contains antibodies against specific RBC antigens. o Incompatible blood is transfused: patient’s antibodies trigger RBC destruction in a potentially dangerous transfusion reaction. o ABO system, which identifies A, B, O, and AB blood types.  Blood type is based on the presence or absence of A and B red blood cell (RBC) antigens  Individuals with type A blood have A antigens on their RBCs and anti-B antibodies in their plasma  Person who has type AB blood has both A and B antigens on the RBCs and no antibodies against either antigen in the plasma  Type O individual has neither A nor B antigens on RBCs but has both anti-A and anti-B antibodies in the plasma)  Type O blood (universal blood donors  Type AB blood (universal blood recipients).  Autologous transfusion (autotransfusion) is the collection and reinfusion of a patient’s own blood. Autologous transfusions are safer for patients because they decrease the risk of mismatched blood and exposure to bloodborne infectious agents.  Severe blood loss (hemorrhage): often receive rapid transfusions through a central venous catheter.

 Personality changes, moon face, increase infection, hyperglycemia, CNS irritability, fluid retention, thin extremities, GI distress, thin skin, purple striae, bruises and petechiae, osteoporosis, fat deposits on face and stomach. Addison’s Syndrome  Adrenocortical Deficit  Bronze skin pigment  Hypoglycemia  Postural hypotension  Weight loss  Weakness  Changes in hair ECV Excess ECV Deficit  Gain of 2.2lbs or more in 24 hours.  Bounding Pulse rate  Full or distended neck veins when upright  Lung auscultation: crackles or rhonchi  Presence of edema  Loss of 2.2lbs or more in 24 hours  Hypotension or OH  Light-headedness on sitting  Rapid an thready pulse  Flat or collapsing neck veins  Sluggish capillary refill  Urine output: small volume of dark urine  Dry mucous membranes  Poor skin turgor  Presence of thirst  Restlessness and confusion.  Metabolic Acidosis: increased rate and depth of respirations  Metabolic Alkalosis: decreased rate and depth of respirations  Muscle weakness: hypo and hyperkalemia  Decreased DTR: Hypercalcemia, hypermagnesemia  Hyperactive Reflexes: Hypocalcemia, hypomagnesemia  Numbness: Hypocalcemia, hypomagnesemia,  Cramps and Tetany: Hypocalcemia, hypomagnesemia,  Tremors: Hypomagnesemia Enteral Fluid Replacement  Oral replacement of fluids is contraindicated when a patient has a mechanical obstruction of the GI tract, has severe nausea, is at high risk for aspiration, or has impaired swallowing.  Strategies to encourage fluid intake include offering frequent small sips of fluid, popsicles, and ice chips.  When replacing fluids by mouth in a patient with ECV deficit, choose fluids that contain sodium.  A feeding tube is appropriate when a patient’s GI tract is healthy but oral fluids cannot be ingested.  Options for administering fluids include gastrostomy or jejunostomy instillations or infusions through small-bore nasogastric feeding tubes. Restriction of Fluids

 Patients who have very severe ECV excess sometimes have both sodium and fluid restrictions.  Patients on fluid restriction need frequent mouth care to moisten mucous membranes, decrease the chance of mucosal drying and cracking, and maintain comfort. Parenteral Fluid Replacement  Fluids and electrolytes may be replaced through infusion of fluids directly into veins (intravenously) rather than via the digestive system.  Parenteral replacement includes parenteral nutrition (PN), IV fluid and electrolyte therapy (crystalloids), and blood and blood component (colloids) administration.  IV devices are called peripheral IVs when the catheter tip lies in a vein in one of the extremities; they are called central venous catheters (CVCs) or IVs when the catheter tip lies in the central circulatory system.  Parenteral nutrition. o IV administration of a complex, highly concentrated solution containing nutrients and electrolytes that is formulated to meet a patient’s needs.  Intravenous therapy (crystalloids). o Goal of IV fluid administration is to correct or prevent fluid and electrolyte disturbances. It allows for direct access to the vascular system, permitting the continuous infusion of fluids over a period of time. Solution Concentration in IV Effective Concentration in Body Comments Dextrose (Glucose) in Water Solutions D5W Isotonic Hypotonic  Isotonic first enters vein; enters rapidly leaving free water; dilutes ECF; water enters cells by osmosis. D10W Hypertonic Hypotonic  Hyper first enters vein; enters rapidly, leaving free water, dilutes ECF, water enters cells. Saline (NaCl) in Water Solutions 0.225% NS (1/4) Hypotinic Hypotonic  Expands ECV and rehydrates cells 0.45% NS (1/2) Hypotonic Hypotonic  Expands ECV and rehydrates cells 0.9% NS Isotonic Isotonic  Expands ECV and does not enter cells. 3% or 5% NaCl Hypertonic Hypertonic  Draws out water from cells into ECF Dextrose in Saline Solutions D50.45%NaCl Hypertonic Hypotonic  Enters cells rapidly, leaving NaCl D50.9%NaCl Hypertonic Isotonic  Enters cells rapidly, leaving NaCl Multiple Electrolyte Solutions Lactated Ringe Isotonic Isotonic  Liver metabolizes to HCO3; expands ECV; does not enter cells

 Equipment o Short-peripheral IV start kit o Smallest gauge catheter (20-24) o Gloves o Short extension tubing o 10-ml syringe  Obtain data from patient’s EHR or perform physical examination of clinical factors/conditions that will respond to or be affected by administration of IV solutions. o Body Weight o Clinical Markers of Vascular Volume  Urine output (decreased, dark yellow)  VS (BP, PR, RR, Temp)  JVD : flat or collapsing with inhalation when supine with ECV deficit; full when upright or semi-upright with ECV excess.  Lungs Auscultated: Crackles or rhonchi in dependent parts of lung may signal fluid buildup caused by ECV excess  Capillary Refill o Clinical Markers of Interstitial Volume  Turgor: more than 2 FVD  Edema: retention  Oral Mucous Membrane: dry ECV o Thirst o Level of Consciousness  Assess available laboratory data (e.g., hematocrit, serum electrolytes, ABGs, and kidney functions [blood urea nitrogen, urine specific gravity, and urine osmolality]).  Prepare short extension tubing with fused needleless connector or separate needleless connector (injection cap) to attach to catheter hub. o Remove protective cap from needleless connector and attach syringe with 1 to 3 mL 0.9% sodium chloride (normal saline [NS]), maintaining sterility. Slowly inject enough saline to prime (fill) short extension tubing and connector, removing all air. Leave syringe attached to tubing. o Adhere to standard ANTT®, maintaining sterility of end of connector by reapplying end caps, and set aside for attaching to catheter hub after successful venipuncture. Do not overtighten end caps.  Prepare IV tubing and solution for continuous infusion o Open IV infusion set, maintaining sterility. o Place roller clamp about 2 to 5 cm below drip chamber and move roller clamp to “off” position (see illustration B). o Remove protective sheath over IV tubing port on plastic IV solution bag o Remove protective cover from IV tubing spike while maintaining sterility of spike. Insert spike into port of IV bag using a twisting motion o Compress drip chamber and release, allowing it to fill one-third to one-half full o Prime air out of IV tubing by filling with IV solution: Remove protective cover on end of IV tubing (some tubing can be primed without removing protective cover) and slowly open roller clamp to allow fluid to flow from drip chamber to distal end of IV tubing.

o Be certain that IV tubing is clear of air and air bubbles. To remove small air bubbles, firmly tap tubing where they are located. Air bubbles will ascend to drip chamber. Check entire length of tubing to ensure that all air bubbles are removed  Apply tourniquet around upper arm about 10 to 15 cm (4–6 inches) above proposed insertion site  Select a venous site most likely to last the full length of the prescribed therapy (Use most distal site in nondominant arm if possible.)  When selecting a vein: o Avoid:  Area of joint flexion  Area with pain on palpation  Site distal to previous venipuncture site  Compromised skin  Location that interferes with planned procedures  Veins that are compromised (upper extremity on side of breast surgery with axillary node dissection or lymphedema or after radiation, arteriovenous [AV] fistulas/grafts, or affected extremity from cerebrovascular accident [CVA])  Place adapter end of short extension set (prepared in Step 3) or needleless connector (injection cap) for saline lock nearby in sterile package.  Perform venipuncture. Anchor vein below anticipated insertion site by placing thumb over vein 4 to 5 cm (1½–2 inches) distal to site and gently stretching skin against direction of insertion. Instruct patient to relax hand or arm.  Warn patient of a sharp stick. Hold VAD with needle bevel up. Align catheter on top of vein at 10- to 30-degree angle. Puncture skin and anterior vein wall  Observe for blood return in catheter or flashback chamber of catheter, indicating that bevel of needle has entered vein. Advance VAD approximately ¼ inch (0.6 cm) into vein and loosen stylet (needle) of the catheter, advance catheter off needle into vein until hub rests at venipuncture site.  Apply gentle but firm pressure with middle finger of nondominant hand 3 cm (1¼ inches) above insertion site. Keep catheter stable with index finger.  Quickly connect Luer-Lok end of short extension tubing with needleless connector to end of catheter hub. Secure connection. Avoid touching sterile connection ends. 1. An IV fluid is infusing more slowly than ordered. The infusion pump is set correctly. Which factors could cause this slowing? (Select all that apply.) 1. Infiltration at VAD site 2. Patient lying on tubing 3. Roller clamp wide open 4. Tubing kinked in bedrails 5. Circulatory overload 2. The nurse assesses pain and redness at a VAD site. Which action is taken first? 1. Apply a warm, moist compress.