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Slide 1-

Fluid, Electrolyte and Acid-Base Balance By Linda A. Martin, EdD, MSN APRN, BC, CNE
Slide 2-

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Slide 3-

Fluid Balance
Slide 4-

General Concepts Intake = Output = Fluid Balance Sensible losses Urination Defecation Wound drainage Insensible losses Evaporation from skin Respiratory loss from lungs
Slide 5-

Fluid Compartments Intracellular 40% of body weight Extracellular 20% of body weight Two types INTERSTITIAL (between) INTRAVASCULAR (inside)
Slide 6-

Age-Related Fluid Changes Full-term baby - 80% Lean Adult Male - 60% Aged client - 40%
Slide 7-

Fluid and Electrolyte Transport PASSIVE TRANSPORT SYSTEMS Diffusion Filtration Osmosis ACTIVE TRANSPORT SYSTEM Pumping Requires energy expenditure
Slide 8-

Diffusion Molecules move across a biological membrane from an area of higher to an area of lower concentration Membrane types Permeable Semi-permeable Impermeable
Slide 9-

Filtration Movement of solute and solvent across a membrane caused by hydrostatic (water pushing) pressure Occurs at the capillary level If normal pressure gradient changes (as occurs with right-sided heart failure) edema results from “third spacing”
Slide 10-

Osmosis Movement of solvent from an area of lower solute concentration to one of higher concentration Occurs through a semipermeable membrane using osmotic (water pulling) pressure
Slide 11-

Active Transport System Solutes can be moved against a concentration gradient Also called “pumping” Dependent on the presence of ATP
Slide 12-

Fluid Types Isotonic Hypotonic Hypertonic
Slide 13-

Isotonic Solution No fluid shift because solutions are equally concentrated Normal saline solution (0.9% NaCl)
Slide 14-

Hypotonic Solution Lower solute concentration Fluid shifts from hypotonic solution into the more concentrated solution to create a balance (cells swell) Half-normal saline solution (0.45% NaCl)
Slide 15-

Hypertonic Solution Higher solute concentration Fluid is drawn into the hypertonic solution to create a balance (cells shrink) 5% dextrose in normal saline (D5/0.9% NaCl)
Slide 16-

Regulatory Mechanisms Baroreceptor reflex Volume receptors Renin-angiotensin-aldosterone mechanism Antidiuretic hormone
Slide 17-

Baroreceptor Reflex Respond to a fall in arterial blood pressure Located in the atrial walls, vena cava, aortic arch and carotid sinus Constricts afferent arterioles of the kidney resulting in retention of fluid
Slide 18-

Volume Receptors Respond to fluid excess in the atria and great vessels Stimulation of these receptors creates a strong renal response that increases urine output
Slide 19-

Renin-Angiotensin-Aldosterone Renin Enzyme secreted by kidneys when arterial pressure or volume drops Interacts with angiotensinogen to form angiotensin I (vasoconstrictor)
Slide 20-

Renin-Angiotensin-Aldosterone Angiotensin Angiotensin I is converted in lungs to angiotensin II using ACE (angiotensin converting enzyme) Produces vasoconstriction to elevate blood pressure Stimulates adrenal cortex to secrete aldosterone
Slide 21-

Renin-Angiotensin-Aldosterone Aldosterone Mineralocorticoid that controls Na+ and K+ blood levels Increases Cl- and HCO3- concentrations and fluid volume
Slide 22-

Aldosterone Negative Feedback Mechanism ECF & Na+ levels drop  secretion of ACTH by the anterior pituitary  release of aldosterone by the adrenal cortex  fluid and Na+ retention
Slide 23-

Antidiuretic Hormone Also called vasopressin Released by posterior pituitary when there is a need to restore intravascular fluid volume Release is triggered by osmoreceptors in the thirst center of the hypothalamus Fluid volume excess  decreased ADH Fluid volume deficit  increased ADH
Slide 24-

Fluid Imbalances Dehydration Hypovolemia Hypervolemia Water intoxication
Slide 25-

Dehydration Loss of body fluids  increased concentration of solutes in the blood and a rise in serum Na+ levels Fluid shifts out of cells into the blood to restore balance Cells shrink from fluid loss and can no longer function properly
Slide 26-

Clients at Risk Confused Comatose Bedridden Infants Elderly Enterally fed
Slide 27-

What Do You See? Irritability Confusion Dizziness Weakness Extreme thirst  urine output Fever Dry skin/mucous membranes Sunken eyes Poor skin turgor Tachycardia
Slide 28-

What Do We Do? Fluid Replacement - oral or IV over 48 hrs. Monitor symptoms and vital signs Maintain I&O Maintain IV access Daily weights Skin and mouth care
Slide 29-

Hypovolemia Isotonic fluid loss from the extracellular space Can progress to hypovolemic shock Caused by: Excessive fluid loss (hemorrhage) Decreased fluid intake Third space fluid shifting
Slide 30-

What Do You See? Mental status deterioration Thirst Tachycardia Delayed capillary refill Orthostatic hypotension Urine output < 30 ml/hr Cool, pale extremities Weight loss
Slide 31-

What Do We Do? Fluid replacement Albumin replacement Blood transfusions for hemorrhage Dopamine to maintain BP MAST trousers for severe shock Assess for fluid overload with treatment
Slide 32-

Hypervolemia Excess fluid in the extracellular compartment as a result of fluid or sodium retention, excessive intake, or renal failure Occurs when compensatory mechanisms fail to restore fluid balance Leads to CHF and pulmonary edema
Slide 33-

What Do You See? Tachypnea Dyspnea Crackles Rapid, bounding pulse Hypertension S3 gallop Increased CVP, pulmonary artery pressure and pulmonary artery wedge pressure (Swan-Ganz) JVD Acute weight gain Edema
Slide 34-

Edema Fluid is forced into tissues by the hydrostatic pressure First seen in dependent areas Anasarca - severe generalized edema Pitting edema Pulmonary edema
Slide 35-

What Do We Do? Fluid and Na+ restriction Diuretics Monitor vital signs Hourly I&O Breath sounds Monitor ABGs and labs Elevate HOB and give O2 as ordered Maintain IV access Skin & mouth care Daily weights
Slide 36-

Water Intoxication Hypotonic extracellular fluid shifts into cells to attempt to restore balance Cells swell Causes: SIADH Rapid infusion of hypotonic solution Excessive tap water NG irrigation or enemas Psychogenic polydipsia
Slide 37-

What Do You See? Signs and symptoms of increased intracranial pressure Early: change in LOC, N/V, muscle weakness, twitching, cramping Late: bradycardia, widened pulse pressure, seizures, coma
Slide 38-

What Do We Do? Prevention is the best treatment Assess neuro status Monitor I&O and vital signs Fluid restrictions IV access Daily weights Monitor serum Na+ Seizure precautions
Slide 39-

Electrolytes
Slide 40-

Electrolytes Charged particles in solution Cations (+) Anions (-) Integral part of metabolic and cellular processes
Slide 41-

Positive or Negative? Cations (+) Sodium Potassium Calcium Magnesium Anions (-) Chloride Bicarbonate Phosphate Sulfate
Slide 42-

Major Cations EXTRACELLULAR SODIUM (Na+) INTRACELLULAR POTASSIUM (K+)
Slide 43-

Electrolyte Imbalances Hyponatremia/ hypernatremia Hypokalemia/ Hyperkalemia Hypomagnesemia/ Hypermagnesemia Hypocalcemia/ Hypercalcemia Hypophosphatemia/ Hyperphosphatemia Hypochloremia/ Hyperchloremia
Slide 44-

Sodium Major extracellular cation Attracts fluid and helps preserve fluid volume Combines with chloride and bicarbonate to help regulate acid-base balance Normal range of serum sodium 135 - 145 mEq/L
Slide 45-

Sodium and Water If sodium intake suddenly increases, extracellular fluid concentration also rises Increased serum Na+ increases thirst and the release of ADH, which triggers kidneys to retain water Aldosterone also has a function in water and sodium conservation when serum Na+ levels are low
Slide 46-

Sodium-Potassium Pump Sodium (abundant outside cells) tries to get into cells Potassium (abundant inside cells) tries to get out of cells Sodium-potassium pump maintains normal concentrations Pump uses ATP, magnesium and an enzyme to maintain sodium-potassium concentrations Pump prevents cell swelling and creates an electrical charge allowing neuromuscular impulse transmission
Slide 47-

Hyponatremia Serum Na+ level < 135 mEq/L Deficiency in Na+ related to amount of body fluid Several types Dilutional Depletional Hypovolemic Hypervolemic Isovolemic
Slide 48-

Types of Hyponatremia Dilutional - results from Na+ loss, water gain Depletional - insufficient Na+ intake Hypovolemic - Na+ loss is greater than water loss; can be renal (diuretic use) or non-renal (vomiting) Hypervolemic - water gain is greater than Na+ gain; edema occurs Isovolumic - normal Na+ level, too much fluid
Slide 49-

What Do You See? Primarily neurologic symptoms Headache, N/V, muscle twitching, altered mental status, stupor, seizures, coma Hypovolemia - poor skin turgor, tachycardia, decreased BP, orthostatic hypotension Hypervolemia - edema, hypertension, weight gain, bounding tachycardia
Slide 50-

What Do We Do? MILD CASE Restrict fluid intake for hyper/isovolemic hyponatremia IV fluids and/or increased po Na+ intake for hypovolemic hyponatremia SEVERE CASE Infuse hypertonic NaCl solution (3% or 5% NaCl) Furosemide to remove excess fluid Monitor client in ICU
Slide 51-

Hypernatremia Excess Na+ relative to body water Occurs less often than hyponatremia Thirst is the body’s main defense When hypernatremia occurs, fluid shifts outside the cells May be caused by water deficit or over-ingestion of Na+ Also may result from diabetes insipidus
Slide 52-

What Do You See? Think S-A-L-T Skin flushed Agitation Low grade fever Thirst Neurological symptoms Signs of hypovolemia
Slide 53-

What Do We Do? Correct underlying disorder Gradual fluid replacement Monitor for s/s of cerebral edema Monitor serum Na+ level Seizure precautions
Slide 54-

Potassium Major intracellular cation Untreated changes in K+ levels can lead to serious neuromuscular and cardiac problems Normal K+ levels = 3.5 - 5 mEq/L
Slide 55-

Balancing Potassium Most K+ ingested is excreted by the kidneys Three other influential factors in K+ balance : Na+/K+ pump Renal regulation pH level
Slide 56-

Sodium/Potassium Pump Uses ATP to pump potassium into cells Pumps sodium out of cells Creates a balance
Slide 57-

Renal Regulation Increased K+ levels  increased K+ loss in urine Aldosterone secretion causes Na+ reabsorption and K+ excretion
Slide 58-

pH Potassium ions and hydrogen ions exchange freely across cell membranes Acidosis  hyperkalemia (K+ moves out of cells) Alkalosis  hypokalemia (K+ moves into cells)
Slide 59-

Hypokalemia Serum K+ < 3.5 mEq/L Can be caused by GI losses, diarrhea, insufficient intake, non-K+ sparing diuretics (thiazide, furosemide)
Slide 60-

What Do You See? Think S-U-C-T-I-O-N Skeletal muscle weakness U wave (EKG changes) Constipation, ileus Toxicity of digitalis glycosides Irregular, weak pulse Orthostatic hypotension Numbness (paresthesias)
Slide 61-

What Do We Do? Increase dietary K+ Oral KCl supplements IV K+ replacement Change to K+-sparing diuretic Monitor EKG changes
Slide 62-

IV K+ Replacement Mix well when adding to an IV solution bag Concentrations should not exceed 40-60 mEq/L Rates usually 10-20 mEq/hr NEVER GIVE IV PUSH POTASSIUM
Slide 63-

Hyperkalemia Serum K+ > 5 mEq/L Less common than hypokalemia Caused by altered kidney function, increased intake (salt substitutes), blood transfusions, meds (K+-sparing diuretics), cell death (trauma)
Slide 64-

What Do You See? Irritability Paresthesia Muscle weakness (especially legs) EKG changes (tented T wave) Irregular pulse Hypotension Nausea, abdominal cramps, diarrhea
Slide 65-

What Do We Do? Mild Loop diuretics (Lasix) Dietary restriction Moderate Kayexalate Emergency 10% calcium gluconate for cardiac effects Sodium bicarbonate for acidosis
Slide 66-

Magnesium Helps produce ATP Role in protein synthesis & carbohydrate metabolism Helps cardiovascular system function (vasodilation) Regulates muscle contractions
Slide 67-

Hypomagnesemia Serum Mg++ level < 1.5 mEq/L Caused by poor dietary intake, poor GI absorption, excessive GI/urinary losses High risk clients Chronic alcoholism Malabsorption GI/urinary system disorders Sepsis Burns Wounds needing debridement
Slide 68-

What Do You See? CNS Altered LOC Confusion Hallucinations
Slide 69-

What Do You See? Neuromuscular Muscle weakness Leg/foot cramps Hyper DTRs Tetany Chvostek’s & Trousseau’s signs
Slide 70-

What Do You See? Cardiovascular Tachycardia Hypertension EKG changes
Slide 71-

What Do You See? Gastrointestinal Dysphagia Anorexia Nausea/vomiting
Slide 72-

What Do We Do? Mild Dietary replacement Severe IV or IM magnesium sulfate Monitor Neuro status Cardiac status Safety
Slide 73-

Mag Sulfate Infusion Use infusion pump - no faster than 150 mg/min Monitor vital signs for hypotension and respiratory distress Monitor serum Mg++ level q6h Cardiac monitoring Calcium gluconate as an antidote for overdosage
Slide 74-

Hypermagnesemia Serum Mg++ level > 2.5 mEq/L Not common Renal dysfunction is most common cause Renal failure Addison’s disease Adrenocortical insufficiency Untreated DKA
Slide 75-

What Do You See? Decreased neuromuscular activity Hypoactive DTRs Generalized weakness Occasionally nausea/vomiting
Slide 76-

What Do We Do? Increased fluids if renal function normal Loop diuretic if no response to fluids Calcium gluconate for toxicity Mechanical ventilation for respiratory depression Hemodialysis (Mg++-free dialysate)
Slide 77-

Calcium 99% in bones, 1% in serum and soft tissue (measured by serum Ca++) Works with phosphorus to form bones and teeth Role in cell membrane permeability Affects cardiac muscle contraction Participates in blood clotting
Slide 78-

Calcium Regulation Affected by body stores of Ca++ and by dietary intake & Vitamin D intake Parathyroid hormone draws Ca++ from bones increasing low serum levels (Parathyroid pulls) With high Ca++ levels, calcitonin is released by the thyroid to inhibit calcium loss from bone (Calcitonin keeps)
Slide 79-

Hypocalcemia Serum calcium < 8.9 mg/dl Ionized calcium level < 4.5 mg/Dl Caused by inadequate intake, malabsorption, pancreatitis, thyroid or parathyroid surgery, loop diuretics, low magnesium levels
Slide 80-

What Do You See? Neuromuscular Anxiety, confusion, irritability, muscle twitching, paresthesias (mouth, fingers, toes), tetany Fractures Diarrhea Diminished response to digoxin EKG changes
Slide 81-

What Do We Do? Calcium gluconate for postop thyroid or parathyroid client Cardiac monitoring Oral or IV calcium replacement
Slide 82-

Hypercalcemia Serum calcium > 10.1 mg/dl Ionized calcium > 5.1 mg/dl Two major causes Cancer Hyperparathyroidism
Slide 83-

What Do You See? Fatigue, confusion, lethargy, coma Muscle weakness, hyporeflexia Bradycardia  cardiac arrest Anorexia, nausea/vomiting, decreased bowel sounds, constipation Polyuria, renal calculi, renal failure
Slide 84-

What Do We Do? If asymptomatic, treat underlying cause Hydrate the patient to encourage diuresis Loop diuretics Corticosteroids
Slide 85-

Phosphorus The primary anion in the intracellular fluid Crucial to cell membrane integrity, muscle function, neurologic function and metabolism of carbs, fats and protein Functions in ATP formation, phagocytosis, platelet function and formation of bones and teeth
Slide 86-

Hypophosphatemia Serum phosphorus < 2.5 mg/dl Can lead to organ system failure Caused by respiratory alkalosis (hyperventilation), insulin release, malabsorption, diuretics, DKA, elevated parathyroid hormone levels, extensive burns
Slide 87-

What Do You See? Musculoskeletal muscle weakness respiratory muscle failure osteomalacia pathological fractures CNS confusion, anxiety, seizures, coma Cardiac hypotension decreased cardiac output Hematologic hemolytic anemia easy bruising infection risk
Slide 88-

What Do We Do? MILD/MODERATE Dietary interventions Oral supplements SEVERE IV replacement using potassium phosphate or sodium phosphate
Slide 89-

Hyperphosphatemia Serum phosphorus > 4.5 mg/dl Caused by impaired kidney function, cell damage, hypoparathyroidism, respiratory acidosis, DKA, increased dietary intake
Slide 90-

What Do You See? Think C-H-E-M-O Cardiac irregularities Hyperreflexia Eating poorly Muscle weakness Oliguria
Slide 91-

What Do We Do? Low-phosphorus diet Decrease absorption with antacids that bind phosphorus Treat underlying cause of respiratory acidosis or DKA IV saline for severe hyperphosphatemia in patients with good kidney function
Slide 92-

Chloride Major extracellular anion Sodium and chloride maintain water balance Secreted in the stomach as hydrochloric acid Aids carbon dioxide transport in blood
Slide 93-

Hypochloremia Serum chloride < 96 mEq/L Caused by decreased intake or decreased absorption, metabolic alkalosis, and loop, osmotic or thiazide diuretics
Slide 94-

What Do You See? Agitation, irritability Hyperactive DTRs, tetany Muscle cramps, hypertonicity Shallow, slow respirations Seizures, coma Arrhythmias
Slide 95-

What Do We Do? Treat underlying cause Oral or IV replacement in a sodium chloride or potassium chloride solution
Slide 96-

Hyperchloremia Serum chloride > 106 mEq/L Rarely occurs alone Caused by dehydration, renal failure, respiratory alkalosis, salicylate toxicity, hyperpara-thyroidism, hyperaldosteronism, hypernatremia
Slide 97-

What Do You See? Metabolic Acidosis Decreased LOC Kussmaul’s respirations Weakness Hypernatremia Agitation Tachycardia, dyspnea, tachypnea, HTN Edema
Slide 98-

What Do We Do? Correct underlying cause Restore fluid, electrolyte and acid-base balance IV Lactated Ringer’s solution to correct acidosis
Slide 99-

Acid-Base Balance
Slide 100-

Acid-Base Basics Balance depends on regulation of free hydrogen ions Concentration of hydrogen ions is measured in pH Arterial blood gases are the major diagnostic tool for evaluating acid-base balance
Slide 101-

Arterial Blood Gases pH 7.35 - 7.45 PaCO2 35 - 45 mmHg HCO3 22-26 mEq/L
Slide 102-

Acidosis pH < 7.35 Caused by accumulation of acids or by a loss of bases
Slide 103-

Alkalosis pH > 7.45 Occurs when bases accumulate or acids are lost
Slide 104-

Regulatory Systems Three systems come into play when pH rises or falls Chemical buffers Respiratory system Kidneys
Slide 105-

Chemical Buffers Immediate acting Combine with offending acid or base to neutralize harmful effects until another system takes over Bicarb buffer - mainly responsible for buffering blood and interstitial fluid Phosphate buffer - effective in renal tubules Protein buffers - most plentiful - hemoglobin
Slide 106-

Respiratory System Lungs regulate blood levels of CO2 CO2 + H2O = Carbonic acid High CO2 = slower breathing (hold on to carbonic acid and lower pH) Low CO2 = faster breathing (blow off carbonic acid and raise pH) Twice as effective as chemical buffers, but effects are temporary
Slide 107-

Kidneys Reabsorb or excrete excess acids or bases into urine Produce bicarbonate Adjustments by the kidneys take hours to days to accomplish Bicarbonate levels and pH levels increase or decrease together
Slide 108-

Arterial Blood Gases (ABG) Uses blood from an arterial puncture Three test results relate to acid-base balance pH PaCO2 HCO3
Slide 109-

Interpreting ABGs Step 1 - check the pH Step 2 - What is the CO2? Step 3 - Watch the bicarb Step 4 - Look for compensation Step 5 - What is the PaO2 and SaO2?
Slide 110-

Step 1 - Check the pH pH < 7.35 = acidosis pH > 7.45 = alkalosis Move on to Step 2
Slide 111-

Step 2 - What is the CO2? PaCO2 gives info about the respiratory component of acid-base balance If abnormal, does the change correspond with change in pH? High pH expects low PaCO2 (hypocapnia) Low pH expects high PaCO2 (hypercapnia)
Slide 112-

Step 3 – Watch the Bicarb Provides info regarding metabolic aspect of acid-base balance If pH is high, bicarb expected to be high (metabolic alkalosis) If pH is low, bicarb expected to be low (metabolic acidosis)
Slide 113-

Step 4 – Look for Compensation If a change is seen in BOTH PaCO2 and bicarbonate, the body is trying to compensate Compensation occurs as opposites, (Example: for metabolic acidosis, compensation shows respiratory alkalosis)
Slide 114-

Step 5 – What is the PaO2 and SaO2 PaO2 reflects ability to pickup O2 from lungs SaO2 less than 95% is inadequate oxygenation Low PaO2 indicates hypoxemia
Slide 115-

Acid-Base Imbalances Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis
Slide 116-

Respiratory Acidosis Any compromise in breathing can result in respiratory acidosis Hypoventilation carbon dioxide buildup and drop in pH Can result from neuromuscular trouble, depression of the brain’s respiratory center, lung disease or airway obstruction
Slide 117-

Clients At Risk Post op abdominal surgery Mechanical ventilation Analgesics or sedation
Slide 118-

What Do You See? Apprehension, restlessness Confusion, tremors Decreased DTRs Diaphoresis Dyspnea, tachycardia N/V, warm flushed skin
Slide 119-

ABG Results Uncompensated pH < 7.35 PaCO2 >45 HCO3 Normal Compensated pH Normal PaCO2 >45 HCO3 > 26
Slide 120-

What Do We Do? Correct underlying cause Bronchodilators Supplemental oxygen Treat hyperkalemia Antibiotics for infection Chest PT to remove secretions Remove foreign body obstruction
Slide 121-

Respiratory Alkalosis Most commonly results from hyperventilation caused by pain, salicylate poisoning, use of nicotine or aminophylline, hypermetabolic states or acute hypoxia (overstimulates the respiratory center)
Slide 122-

What Do You See? Anxiety, restlessness Diaphoresis Dyspnea ( rate and depth) EKG changes Hyperreflexia, paresthesias Tachycardia Tetany
Slide 123-

ABG Results Uncompensated pH > 7.45 PaCO2 < 35 HCO3 Normal Compensated pH Normal PaCO2 < 35 HCO3 < 22
Slide 124-

What Do We Do? Correct underlying disorder Oxygen therapy for hypoxemia Sedatives or antianxiety agents Paper bag breathing for hyperventilation
Slide 125-

Metabolic Acidosis Characterized by gain of acid or loss of bicarb Associated with ketone bodies Diabetes mellitus, alcoholism, starvation, hyperthyroidism Other causes Lactic acidosis secondary to shock, heart failure, pulmonary disease, hepatic disease, seizures, strenuous exercise
Slide 126-

What Do You See? Confusion, dull headache Decreased DTRs S/S hyperkalemia (abdominal cramps, diarrhea, muscle weakness, EKG changes) Hypotension, Kussmaul’s respirations Lethargy, warm & dry skin
Slide 127-

ABG Results Uncompensated pH < 7.35 PaCO2 Normal HCO3 < 22 Compensated pH Normal PaCO2 < 35 HCO3 < 22
Slide 128-

What Do We Do? Regular insulin to reverse DKA IV bicarb to correct acidosis Fluid replacement Dialysis for drug toxicity Antidiarrheals
Slide 129-

Metabolic Alkalosis Commonly associated with hypokalemia from diuretic use, hypochloremia and hypocalcemia Also caused by excessive vomiting, NG suction, Cushing’s disease, kidney disease or drugs containing baking soda
Slide 130-

What Do You See? Anorexia Apathy Confusion Cyanosis Hypotension Loss of reflexes Muscle twitching Nausea Paresthesia Polyuria Vomiting Weakness
Slide 131-

ABG Results Uncompensated pH > 7.45 PaCO2 Normal HCO3 >26 Compensated pH Normal PaCO2 > 45 HCO3 > 26
Slide 132-

What Do We Do? IV ammonium chloride D/C thiazide diuretics and NG suctioning Antiemetics
Slide 133-

IV Therapy Crystalloids – volume expander Isotonic (D5W, 0.9% NaCl or Lactated Ringers) Hypotonic (0.45% NaCl) Hypertonic (D5/0.9% NaCl, D5/0.45% NaCl) Colloids – plasma expander (draw fluid into the bloodstream) Albumin Plasma protein Dextran
Slide 134-

Total Parenteral Nutrition Highly concentrated Hypertonic solution Used for clients with high caloric and nutritional needs Solution contains electrolytes, vitamins, acetate, micronutrients and amino acids Lipid emulsions given in addition
Slide 135-

The End (Whew!!!!!!)