Fluid and Electrolytes: Balance and Disturbance

Fluid and Electrolyte Balance Necessary for life, homeostasis Nursing role: help prevent, treat fluid, electrolyte disturbances

Fluid Approximately 60% of typical adult is fluid – Varies with age, body size, gender Intracellular fluid Extracellular fluid – Intravascular – Interstitial – Transcellular “Third spacing”: loss of ECF into space that does not contribute to equilibrium

Electrolytes Active chemicals that carry positive (cations), negative (anions) electrical charges – Major cations: sodium, potassium, calcium, magnesium, hydrogen ions – Major anions: chloride, bicarbonate, phosphate, sulfate, and proteinate ions Electrolyte concentrations differ in fluid compartments

Regulation of Fluid Movement of fluid through capillary walls depends on – Hydrostatic pressure: exerted on walls of blood vessels – Osmotic pressure: exerted by protein in plasma Direction of fluid movement depends on differences of hydrostatic, osmotic pressure

Regulation of Fluid Osmosis: area of low solute concentration to area of high solute concentration Diffusion: solutes move from area of higher concentration to one of lower concentration Filtration: movement of water, solutes occurs from area of high hydrostatic pressure to area of low hydrostatic pressure Active transport: physiologic pump that moves fluid from area of lower concentration of one of higher concentration

Active Transport Physiologic pump that moves fluid from area of lower concentration to one of higher concentration Movement against concentration gradient Sodium-potassium pump: maintains higher concentration of extracellular sodium, intracellular potassium Requires adenosine (ATP) for energy

Routes of Gains and Losses Gain – Dietary intake of fluid, food or enteral feeding – Parenteral fluids

Routes of Gains and Losses (cont’d) Loss – Kidney: urine output – Skin loss: sensible, insensible losses – Lungs – GI tract – Other

Gerontologic Considerations Reduced homeostatic mechanisms: cardiac, renal, respiratory function Decreased body fluid percentage Medication use Presence of concomitant conditions

Fluid Volume Imbalances Fluid volume deficit (FVD): hypovolemia Fluid volume excess (FVE): hypervolemia

Fluid Volume Deficit Loss of extracellular fluid exceeds intake ratio of water – Electrolytes lost in same proportion as they exist in normal body fluids Dehydration: loss of water along with increased serum sodium level – May occur in combination with other imbalances

Fluid Volume Deficit (cont’d) Dehydration – Causes: fluid loss from vomiting, diarrhea, GI suctioning, sweating, decreased intake, inability to gain access to fluid – Risk factors: diabetes insipidus, adrenal insufficiency, osmotic diuresis, hemorrhage, coma, third space shifts

Fluid Volume Deficit (cont’d) Manifestations: rapid weight loss, decreased skin turgor, oliguria, concentrated urine, postural hypotension, rapid weak pulse, increased temperature, cool clammy skin due to vasoconstriction, lassitude, thirst, nausea, muscle weakness, cramps Laboratory data: elevated BUN in relation to serum creatinine, increased hematocrit – Serum electrolyte changes may occur

Fluid Volume Deficit (cont’d) Medical management: provide fluids to meet body needs – Oral fluids – IV solutions

Fluid Volume Deficit - Nursing Management I&O, VS Monitor for symptoms: skin and tongue turgor, mucosa, UO, mental status Measures to minimize fluid loss Oral care Administration of oral fluids Administration of parenteral fluids

Fluid Volume Excess Due to fluid overload or diminished homeostatic mechanisms Risk factors: heart failure, renal failure, cirrhosis of liver Contributing factors: excessive dietary sodium or sodium- containing IV solutions Manifestations: edema, distended neck veins, abnormal lung sounds (crackles), tachycardia, increased BP, pulse pressure and CVP, increased weight, increased UO, shortness of breath and wheezing Medical management: directed at cause, restriction of fluids and sodium, administration of diuretics

Fluid Volume Excess - Nursing Management I&O and daily weights; assess lung sounds, edema, other symptoms; monitor responses to medications- diuretics Promote adherence to fluid restrictions, patient teaching related to sodium and fluid restrictions Monitor, avoid sources of excessive sodium, including medications Promote rest Semi-Fowler’s position for orthopnea Skin care, positioning/turning

Electrolyte Imbalances Sodium: hyponatremia, hypernatremia Potassium: hypokalemia, hyperkalemia Calcium: hypocalcemia, hypercalcemia Magnesium: hypomagnesemia, hypermagnesemia Phosphorus: hypophosphatemia, hyperphosphatemia Chloride: hypochloremia, hyperchloremia

Hyponatremia Serum sodium less than 135 mEq/L Causes: adrenal insufficiency, water intoxication, SIADH or losses by vomiting, diarrhea, sweating, diuretics Manifestations: poor skin turgor, dry mucosa, headache, decreased salivation, decreased BP, nausea, abdominal cramping, neurologic changes Medical management: water restriction, sodium replacement Nursing management: assessment and prevention, dietary sodium and fluid intake, identify and monitor at- risk patients, effects of medications (diuretics, lithium)

Hypernatremia Serum sodium greater than 145mEq/L Causes: excess water loss, excess sodium administration, diabetes insipidus, heat stroke, hypertonic IV solutions Manifestations: thirst; elevated temperature; dry, swollen tongue; sticky mucosa; neurologic symptoms; restlessness; weakness Note: thirst may be impaired in elderly or the ill Medical management: hypotonic electrolyte solution or D5W Nursing management: assessment and prevention, assess for OTC sources of sodium, offer and encourage fluids to meet patient needs, provide sufficient water with tube feedings

Hypokalemia Below-normal serum potassium (<3.5 mEq/L), may occur with normal potassium levels with alkalosis due to shift of serum potassium into cells Causes: GI losses, medications, alterations of acid- base balance, hyperaldosterism, poor dietary intake Manifestations: fatigue, anorexia, nausea, vomiting, dysrhythmias, muscle weakness and cramps, paresthesias, glucose intolerance, decreased muscle strength, DTRs Medical management: increased dietary potassium, potassium replacement, IV for severe deficit Nursing management: assessment, severe hypokalemia is life-threatening, monitor ECG and ABGs, dietary potassium, nursing care related to IV potassium administration

Hyperkalemia Serum potassium greater than 5.0 mEq/L Causes: usually treatment related, impaired renal function, hypoaldosteronism, tissue trauma, acidosis Manifestations: cardiac changes and dysrhythmias, muscle weakness with potential respiratory impairment, paresthesias, anxiety, GI manifestations Medical management: monitor ECG, limitation of dietary potassium, cation-exchange resin (Kayexalate), IV sodium bicarbonate, IV calcium gluconate, regular insulin and hypertonic dextrose IV,  -2 agonists, dialysis

Hyperkalemia (cont’d) Nursing management: assessment of serum potassium levels, mix IVs containing K+ well, monitor medication affects, dietary potassium restriction/dietary teaching for patients at risk Hemolysis of blood specimen or drawing of blood above IV site may result in false laboratory result Salt substitutes, medications may contain potassium Potassium-sparing diuretics may cause elevation of potassium – Should not be used in patients with renal dysfunction

Hypocalcemia Serum level less than 8.5 mg/dL, must be considered in conjunction with serum albumin level Causes: hypoparathyroidism, malabsorption, pancreatitis, alkalosis, massive transfusion of citrated blood, renal failure, medications, other Manifestations: tetany, circumoral numbness, paresthesias, hyperactive DTRs, Trousseau’s sign, Chovstek's sign, seizures, respiratory symptoms of dyspnea and laryngospasm, abnormal clotting, anxiety

Hypocalcemia (cont’d) Medical management: IV of calcium gluconate, calcium and vitamin D supplements; diet Nursing management: assessment, severe hypocalcemia is life-threatening, weight- bearing exercises to decrease bone calcium loss, patient teaching related to diet and medications, and nursing care related to IV calcium administration

Trousseau’s Sign

Hypercalcemia Serum level above 10.5 mg/dL Causes: malignancy and hyperparathyroidism, bone loss related to immobility Manifestations: muscle weakness, incoordination, anorexia, constipation, nausea and vomiting, abdominal and bone pain, polyuria, thirst, ECG changes, dysrhythmias Medical management: treat underlying cause, fluids, furosemide, phosphates, calcitonin, biphosphonates Nursing management: assessment, hypercalcemic crisis has high mortality, encourage ambulation, fluids of 3 to 4 L/d, provide fluids containing sodium unless contraindicated, fiber for constipation, ensure safety

Hypomagnesemia Serum level less than 1.8 mg/dL, evaluate in conjunction with serum albumin Causes: alcoholism, GI losses, enteral or parenteral feeding deficient in magnesium, medications, rapid administration of citrated blood; contributing causes include diabetic ketoacidosis, sepsis, burns, hypothermia Manifestations: neuromuscular irritability, muscle weakness, tremors, athetoid movements, ECG changes and dysrhythmias, alterations in mood and level of consciousness Medical management: diet, oral magnesium, magnesium sulfate IV

Hypomagnesemia (cont’d) Nursing management: assessment, ensure safety, patient teaching related to diet, medications, alcohol use, and nursing care related to IV magnesium sulfate Hypomagnesemia often accompanied by hypocalcemia – Need to monitor, treat potential hypocalcemia Dysphasia common in magnesium-depleted patients – Assess ability to swallow with water before administering food or medications

Hypermagnesemia Serum level more than 2.7 mg/dL Causes: renal failure, diabetic ketoacidosis, excessive administration of magnesium Manifestations: flushing, lowered BP, nausea, vomiting, hypoactive reflexes, drowsiness, muscle weakness, depressed respirations, ECG changes, dysrhythmias Medical management: IV calcium gluconate, loop diuretics, IV NS of RL, hemodialysis Nursing management: assessment, do not administer medications containing magnesium, patient teaching regarding magnesium containing OTC medications

Hypophosphatemia Serum level below 2.5 mg/DL Causes: alcoholism, refeeding of patients after starvation, pain, heat stroke, respiratory alkalosis, hyperventilation, diabetic ketoacidosis, hepatic encephalopathy, major burns, hyperparathyroidism, low magnesium, low potassium, diarrhea, vitamin D deficiency, use of diuretic and antacids Manifestations: neurologic symptoms, confusion, muscle weakness, tissue hypoxia, muscle and bone pain, increased susceptibility to infection Medical management: oral or IV phosphorus replacement Nursing management: assessment, encourage foods high in phosphorus, gradually introduce calories for malnourished patients receiving parenteral nutrition

Hyperphosphatemia Serum level above 4.5 mg/DL Causes: renal failure, excess phosphorus, excess vitamin D, acidosis, hypoparathyroidism, chemotherapy Manifestations: few symptoms; soft-tissue calcifications, symptoms occur due to associated hypocalcemia Medical management: treat underlying disorder, vitamin- D preparations, calcium-binding antacids, phosphate- binding gels or antacids, loop diuretics, NS IV, dialysis Nursing management: assessment, avoid high- phosphorus foods; patient teaching related to diet, phosphate-containing substances, signs of hypocalcemia

Hypochloremia Serum level less than 96 mEq/L Causes: Addison’s disease, reduced chloride intake, GI loss, diabetic ketoacidosis, excessive sweating, fever, burns, medications, metabolic alkalosis Loss of chloride occurs with loss of other electrolytes, potassium, sodium Manifestations: agitation, irritability, weakness, hyperexcitability of muscles, dysrhythmias, seizures, coma Medical management: replace chloride-IV NS or 0.45% NS Nursing management: assessment, avoid free water, encourage high-chloride foods, patient teaching related to high-chloride foods

Hyperchloremia Serum level more than 108 mEq/L Causes: excess sodium chloride infusions with water loss, head injury, hypernatremia, dehydration, severe diarrhea, respiratory alkalosis, metabolic acidosis, hyperparathyroidism, medications Manifestations: tachypnea, lethargy, weakness, rapid, deep respirations, hypertension, cognitive changes Normal serum anion gap Medical management: restore electrolyte and fluid balance, LR, sodium bicarbonate, diuretics Nursing management: assessment, patient teaching related to diet and hydration

Maintaining Acid-Base Balance Normal plasma pH : hydrogen ion concentration Major extracellular fluid buffer system; bicarbonate-carbonic acid buffer system Kidneys regulate bicarbonate in ECF Lungs under control of medulla regulate CO2, carbonic acid in ECF

Maintaining Acid-Base Balance (cont’d) Other buffer systems – ECF: inorganic phosphates, plasma proteins – ICF: proteins, organic, inorganic phosphates – Hemoglobin

ACID–BASE DISTURBANCES Plasma pH is an indicator of hydrogen ion (H+) concentration. Normal range pH (7.35–7.45). Buffer systems – Kidneys – Lungs The H+ concentration is extremely important: – Increased concentration H+ Increased acidity Lower the pH. – Deceased H+ concentration Increased alkalinity Higher the pH. pH range compatible with life (6.8–7.8)

BUFFER SYSTEMS Buffer systems prevent major changes in the pH of body fluids Both intracellular and extracellular buffers. – Major extracellular buffer system is Bicarbonate-carbonic acid – Assessed when arterial blood gases are measured. Normally, there are 20 parts of bicarbonate (HCO3−) to one part of carbonic acid (H2CO3). If this ratio is altered, the pH will change. The ratio which maintains pH, not absolute values. Carbon dioxide (CO2) is a potential acid; when dissolved in water, it becomes carbonic acid (CO2 + H2O = H2CO3). Thus, when CO2 is increased, the carbonic acid is also increased Changes in and H2CO3 concentration results in acid–base imbalances. – Intracellular buffers are proteins, organic and inorganic phosphates – Hemoglobin.

KIDNEYS Regulate the bicarbonate level in the ECF Can regenerate and reabsorb HCO3− In respiratory acidosis and most cases of metabolic acidosis Kidneys excrete H+ and conserve HCO3− In respiratory and metabolic alkalosis – Kidneys retain H+ and excrete HCO3− Kidneys cannot compensate for the metabolic acidosis created by RF Renal compensation is relatively slow (a matter of hours or days).

LUNGS Control PaCO2 and thus the H2CO3 of ECF. A rise PaCO2 is a powerful stimulant to respiration. PaO2 also influences respiration, But PaCO2 is stronger In metabolic acidosis – Respiratory rate increases to eliminate CO2 (to reduce acid). In metabolic alkalosis – Respiratory rate decreases to retain CO2 (to increase acid).

Metabolic Acidosis Low pH <7.35 Low bicarbonate <22 mEq/L Most commonly due to renal failure Manifestations: headache, confusion, drowsiness, increased respiratory rate and depth, decreased blood pressure, decreased cardiac output, dysrhythmias, shock; if decrease is slow, patient may be asymptomatic until bicarbonate is 15 mEq/L or less Correct underlying problem, correct imbalance – Bicarbonate may be administered

Metabolic Acidosis (cont’d) With acidosis, hyperkalemia may occur as potassium shifts out of cell As acidosis is corrected, potassium shifts back into cell, potassium levels decrease Monitor potassium levels Serum calcium levels may be low with chronic metabolic acidosis – Must be corrected before treating acidosis

Metabolic Alkalosis High pH >7.45 High bicarbonate >26 mEq/L Most commonly due to vomiting or gastric suction – May also be due to medications, especially long-term diuretic use Hypokalemia will produce alkalosis Manifestations: symptoms related to decreased calcium, respiratory depression, tachycardia, symptoms of hypokalemia

Metabolic Alkalosis (cont’d) Correct underlying disorder, supply chloride to allow excretion of excess bicarbonate, restore fluid volume with sodium chloride solutions

Respiratory Acidosis Low pH <7.35 PaCO2 >42 mm Hg Always due to respiratory problem with inadequate excretion of CO2 With chronic respiratory acidosis, body may compensate, may be asymptomatic – Symptoms may be suddenly increased pulse, respiratory rate and BP, mental changes, feeling of fullness in head

Respiratory Acidosis (cont’d) Potential increased intracranial pressure Treatment aimed at improving ventilation

Respiratory Alkalosis High pH >7.45 PaCO2 <35 mm Hg Always due to hyperventilation Manifestations: lightheadedness, inability to concentrate, numbness and tingling, sometimes loss of consciousness Correct cause of hyperventilation

MIXED ACID–BASE DISORDERS At times patients can simultaneously experience two or more independent acid–base disorders. A normal pH in the presence of changes in the PaCO2 and plasma HCO3− concentration immediately suggests a mixed disorder. The only mixed disorder that cannot occur is a mixed respiratory acidosis and alkalosis, because it is impossible to have alveolar hypoventilation and hyperventilation at the same time. An example of a mixed disorder is the simultaneous occurrence of metabolic acidosis and respiratory acidosis during respiratory and cardiac arrest.

COMPENSATION Generally, the pulmonary and renal systems compensate for each other to return the pH to normal. In a single acid–base disorder, the system not causing the problem will try to compensate by returning the ratio of bicarbonate to carbonic acid to the normal 20:1. The lungs compensate for metabolic disturbances by changing CO2 excretion. The kidneys compensate for respiratory disturbances by altering bicarbonate retention and H+ secretion. In respiratory acidosis, excess hydrogen is excreted in the urine in exchange for bicarbonate ions. In respiratory alkalosis, the renal excretion of bicarbonate increases, and hydrogen ions are retained. In metabolic acidosis, the compensatory mechanisms increase the ventilation rate and the renal retention of bicarbonate. In metabolic alkalosis, the respiratory system compensates by decreasing ventilation to conserve CO2 and raise the PaCO2. Because the lungs respond to acid–base disorders within minutes, compensation for metabolic imbalances occurs faster than compensation for respiratory imbalances. Table 14-7 summarizes compensation effects.

Arterial Blood Gases pH (7.4) PaCO (40) - 45 mm Hg HCO3ˉ 22 - (24) - 26 mEq/L – Assumed average values for ABG interpretation PaO2 80 to 100 mm Hg Oxygen saturation >94% Base excess/deficit ±2 mEq/L

ACID–BASE DISTURBANCES AND COMPENSATION DISORDER INITIAL EVENT COMPENSATION Respiratory acidosis↑ PaCO2, ↑ or normal Kidneys eliminate H+ and HCO3 −, ↓ pHretain HCO3− Respiratory alkalosis↓ PaCO2, ↓ or normalKidneys conserve H+ and HCO3−, ↑ pHexcrete HCO3− Metabolic acidosis↓ or normal PaCO2, Lungs eliminate CO2, ↓ HCO3−, ↓ pHconserve HCO3− Metabolic alkalosis↑ or normal PaCO2, Lungs ↓ ventilation to↑ ↑ HCO3−, ↑ pHPCO2, kidneys conserve H+ to excrete HCO3−

IV Site Selection

Complications of IV Therapy Fluid overload Air embolism Septicemia, other infections Infiltration, extravasation Phlebitis Thrombophlebitis Hematoma Clotting, obstruction