RC

Fluid, Electrolyte, and Acid-Base Imbalances

CHAPTER 17: Fluid, Electrolyte, and Acid-Base Imbalances

Normal Physiology

  • Homeostasis is maintained by keeping the composition and volume of fluids and electrolytes within narrow limits.

  • Fluid and electrolyte imbalances are common in patients with major illnesses or injuries.

  • Imbalances are classified as deficits or excesses.

Water Content of the Body

  • Water content varies with body mass, gender, and age.

  • Lean body mass has a higher percentage of water.

  • Fat tissue has a lower percentage of water.

  • Adult body weight is 50-60% water.

Body Fluid Compartments

  • Intracellular Fluid (ICF): 28 L

  • Extracellular Fluid (ECF)

    • Plasma: 3 L

    • Interstitial Fluid (IF): 10 L

Calculation of Fluid Gain or Loss

  • 1 L of water weighs 2.2 pounds (1 kg).

  • Body weight change is a good indicator of overall fluid volume loss or gain.

Electrolytes

  • Substances that dissociate into ions when placed in water.

  • Cations: positively charged ions.

  • Anions: negatively charged ions.

  • Electrolyte concentration is expressed in milliequivalents (mEq)/L.

Electrolyte Composition

  • ICF

    • Prevalent cation: K^+ potassium

    • Prevalent anion: PO_4^{3-} phos

  • ECF

    • Prevalent cation: Na^+ ssodium

    • Prevalent anion: Cl^- chloride

Concentrations of Cations and Anions

  • Refer to the provided diagrams for specific concentrations of cations and anions in plasma and intracellular fluid (ICF).

Mechanisms Controlling Fluid and Electrolyte Movement

  • Diffusion: Movement of molecules from an area of high concentration to an area of low concentration.

  • Active Transport: Requires energy (ATP) to move electrolytes against a concentration gradient (e.g., sodium-potassium pump).

  • Osmosis: Movement of water across a semipermeable membrane from an area of low solute concentration to an area of high solute concentration.

Osmotic Pressure

  • The osmolality of fluid surrounding cells affects them.

    • Isotonic: Same solute concentration as the cell interior.

    • Hypotonic: Lower solute concentration than the cell interior (hypoosmolar).

    • Hypertonic: Higher solute concentration than the cell interior (hyperosmolar).

Osmotic Movement of Fluids

  • Plasma Osmolality Calculation:

    • Plasma\ Osmolality = (2 \times Na) + (BUN / 2.8) + (glucose / 18)

    • Normal plasma osmolality: 280-295 mOsm/kg

    • Greater than 295 mOsm/kg: water deficit

    • Less than 275 mOsm/kg: water excess

Hydrostatic and Oncotic Pressure

  • Hydrostatic Pressure: Force of fluid in a compartment; blood pressure generated by the heart's contraction.

  • Oncotic Pressure: Colloid osmotic pressure; osmotic pressure caused by plasma proteins.

Fluid Movement in Capillaries

  • Determined by:

    • Capillary hydrostatic pressure

    • Plasma oncotic pressure

    • Interstitial hydrostatic pressure

    • Interstitial oncotic pressure

Fluid Shifts

  • Edema is caused by:

    • Shifts of plasma to interstitial fluid

    • Elevation of venous hydrostatic pressure

    • Decrease in plasma oncotic pressure

    • Elevation of interstitial oncotic pressure

Fluid Spacing

  • First Spacing: Normal distribution in ICF and ECF.

  • Second Spacing: Abnormal accumulation of interstitial fluid (edema).

  • Third Spacing: Fluid trapped where it's difficult or impossible to move back into cells or blood vessels.

Regulation of Water Balance

  • Hypothalamic-Pituitary Regulation

    • Osmoreceptors in hypothalamus sense fluid deficit or increase.

    • Deficit stimulates thirst and antidiuretic hormone (ADH) release.

    • Decreased plasma osmolality (water excess) suppresses ADH release.

  • Renal Regulation

    • Main organ for regulating fluid and electrolyte balance.

    • Adjusts urine volume.

    • Selective reabsorption of water and electrolytes.

    • Renal tubules are sites of action of ADH and aldosterone.

  • Adrenal Cortical Regulation

    • Releases hormones to regulate water and electrolytes.

    • Glucocorticoids (e.g., cortisol).

    • Mineralocorticoids (e.g., aldosterone).

Factors Affecting Aldosterone Secretion

  • Renal perfusion:

    • ↓Renal perfusion → ↑ Renin secretion → ↑ Plasma angiotensin II → ↑ Aldosterone secretion

  • Other factors:

    • Stress, physical trauma, ↑ Serum K^+, ↓ Serum Na^+, ↑ ACTH

Effects of Stress on Fluid and Electrolyte Balance

  • Stress → Hypothalamus (CRH) → Anterior pituitary (↑ ACTH secretion) + Posterior pituitary (↑ ADH secretion).

  • Adrenal cortex (↑ Aldosterone, ↑ Cortisol) → Kidney (↑ Na^+ reabsorption, ↑ K^+ excretion, ↑ H_2O reabsorption)

Regulation of Water Balance (Continued)

  • Cardiac Regulation

    • Natriuretic peptides are antagonists to the RAAS.

    • Hormones made by cardiomyocytes in response to increased atrial pressure.

    • They suppress secretion of aldosterone, renin, and ADH to decrease blood volume and pressure.

  • GI Regulation

    • Oral intake accounts for most water.

    • Small amounts of water are eliminated by GI tract in feces.

    • Diarrhea and vomiting can lead to significant fluid and electrolyte loss.

Gerontologic Considerations

  • Structural changes in kidneys decrease ability to conserve water.

  • Hormonal changes include a decrease in renin and aldosterone and increase in ADH and ANP.

  • Subcutaneous tissue loss leads to increased moisture lost.

Fluid Volume Imbalances

  • Fluid Volume Deficit (FVD) or Hypovolemia

    • Abnormal loss of body fluids, inadequate fluid intake, or plasma to interstitial fluid shift.

    • Dehydration: Loss of pure water without a corresponding loss of sodium.

    • FVD Interprofessional Care: Correct underlying cause and replace water and electrolytes (orally, blood products, isotonic IV solutions).

  • Fluid Volume Excess (Hypervolemia)

    • Excess fluid intake, abnormal fluid retention, or interstitial-to-plasma fluid shift.

    • Clinical manifestations related to excess volume (weight gain is the most common).

    • Interprofessional Care: Remove fluid without changing electrolyte composition or osmolality of ECF (diuretics, fluid restriction, possible sodium restriction, removal of fluid to treat ascites or pleural effusion).

Nursing Management: Fluid Imbalances

  • Assessment:

    • Health history (kidney, heart, GI, or respiratory problems).

    • Prior fluid balance problems.

    • Recent changes in body weight.

    • Exercise pattern/activity level.

    • Current and past medications.

    • Dialysis or surgeries.

    • Monitor laboratory results when available.

  • Clinical Problems:

    • Hypervolemia, hypovolemia

    • Deficient knowledge- fluid volume management

    • Impaired tissue perfusion

    • Altered blood pressure

    • Impaired respiratory system function

    • Impaired urinary system function

    • Risk for injury

    • Risk for impaired skin integrity

  • Implementation:

    • Daily weights, I & O

    • Cardiovascular care, respiratory care

    • Patient safety, skin care

Assessment of Skin Turgor

  • Refer to the provided images for assessing skin turgor.

Fluid Therapy

  • Give IV fluids as ordered.

  • Carefully monitor rate of infusion.

  • Maintain adequate oral intake.

  • Assess ability to obtain adequate fluids independently, express thirst, and swallow effectively.

  • Assist those with physical limitations.

Sodium

  • Imbalances typically associated with parallel changes in osmolality.

  • Plays a major role in ECF volume and concentration, generating and transmitting nerve impulses, muscle contractility, and regulating acid-base balance.

Hypernatremia

  • High serum sodium may occur with inadequate water intake, excess water loss, or sodium gain.

  • Causes hyperosmolality leading to cellular dehydration.

  • Primary protection is thirst.

  • Clinical manifestations: thirst, changes in mental status (drowsiness, restlessness, confusion, lethargy, seizures, coma), symptoms of fluid volume deficit.

  • Treatment: Treat underlying cause.

Differential Assessment of ECF Volume

  • Extracellular contraction (Volume deficit resulting from H_2O deficiency): Hypernatremia

  • Normal: Isotonic ECF deficit (Normal Na^+)

  • Extracellular expansion (Volume excess resulting from H_2O excess): Hyponatremia

  • Normal: Isotonic ECF excess (Normal Na^+)

Imbalances in ECF Volume

  • Net loss > H_2O loss: Hypoosmolar imbalance

  • Sodium and water: Isotonic loss (Osmolar balance)

  • H_2O loss > Na^+ loss: Hyperosmolar imbalance

  • Net gain > H_2O gain: Hyperosmolar imbalance

  • Sodium and water: Isotonic gain (Osmolar balance)

  • H_2O gain > Na^+ gain: Hypoosmolar imbalance

Hyponatremia

  • Results from loss of sodium-containing fluids and/or from water excess.

  • Clinical manifestations: Mild (headache, irritability, difficulty concentrating); More severe (confusion, vomiting, seizures, coma).

  • If the cause is water excess:

    • Fluid restriction may be the only treatment

    • Loop diuretics and demeclocycline.

    • Severe symptoms (seizures): Give small amount of IV hypertonic saline solution (3% NaCl).

  • If the cause is abnormal fluid loss:

    • Fluid replacement with isotonic sodium-containing solution.

    • Encouraging oral intake.

    • Withholding diuretics.

    • Drugs that block vasopressin (ADH): Convaptan (Vaprisol) IV, Tolvaptan (Samsca) oral.

Potassium

  • Major ICF cation.

  • Necessary for resting membrane potential of nerve and muscle cells, regulating intracellular osmoality, promoting cellular growth, maintenance of cardiac rhythms, and acid-base balance.

  • Sources: Protein-rich foods, fruits and vegetables, salt substitutes, potassium medications (PO, IV), stored blood.

  • Regulated by kidneys.

Hyperkalemia

  • High serum potassium caused by impaired renal excretion, shift from ICF to ECF, massive intake of potassium, some drugs.

  • Most common in renal failure.

  • Manifestations: Life-threatening arrhythmias, fatigue, confusion, tetany, muscle cramps, weak or paralyzed skeletal muscles, abdominal cramping or diarrhea.

ECG Effects of Hyperkalemia

  • Tall, peaked T wave.

  • Prolonged PR interval.

  • Widened QRS.

  • Depressed ST segment.

  • Wide, flat P wave.

Nursing and Interprofessional Management of Hyperkalemia

  • Stop oral and IV K^+ intake.

  • Increase K^+ excretion (thiazide diuretics, dialysis).

  • patiromer (Veltessa), sodium zirconium cyclosilicate (ZS-9, Lokelma), and/or sodium polystyrene sulfonate (Kayexalate).

  • Force K^+ from ECF to ICF by IV regular insulin with dextrose and a b-adrenergic agonist or sodium bicarbonate.

  • Stabilize cardiac cell membrane by administering calcium chloride or calcium gluconate IV.

  • Use continuous ECG monitoring.

Hypokalemia

  • Low serum potassium caused by increased loss of K^+ via the kidneys or gastrointestinal tract, increased shift of K^+ from ECF to ICF, decreased dietary K^+ (rare).

  • Renal losses from loop or potassium-depleting diuresis

  • Low magnesium level.

  • Clinical manifestations: Cardiac most serious, skeletal muscle weakness and paresthesia, weakness of respiratory muscles, decreased GI motility, hyperglycemia.

ECG Effects of Hypokalemia

  • Slightly prolonged PR interval.

  • ST depression.

  • Slightly peaked P wave.

  • Shallow T wave.

  • Prominent U wave.

  • Decreased R wave amplitude.

Nursing and Interprofessional Management of Hypokalemia

  • KCl supplements orally or IV.

  • Always dilute IV KCl.

  • NEVER give KCl via IV push or as a bolus.

  • Should not exceed 10 mEq/hr.

  • Use an infusion pump.

Calcium

  • Functions: Formation of teeth and bone, blood clotting, transmission of nerve impulses, myocardial contractions, muscle contractions.

  • Major source is dietary intake. Need vitamin D to absorb.

  • Present in bones and plasma. Ionized or free calcium is biologically active.

  • Changes in pH and serum albumin affect levels.

  • Balance controlled by parathyroid hormone (PTH) and calcitonin.

    • Parathyroid hormone (PTH): Increases bone resorption, GI absorption, and renal tubule reabsorption of calcium.

    • Calcitonin: Increases calcium deposition into bone, increases renal calcium excretion, and decreases GI absorption.

Hypercalcemia

  • High levels of serum calcium caused by hyperparathyroidism (two-thirds of cases), cancers, especially kidney, breast, prostate, ovarian, hematologic, and lung cancers.

  • Manifestations: Fatigue, lethargy, weakness, confusion, hallucinations, seizures, coma, dysrhythmias, bone pain, fractures, nephrolithiasis, polyuria, dehydration.

Nursing and Interprofessional Management of Hypercalcemia

  • Low calcium diet.

  • Stop medications related to hypercalcemia.

  • Increased weight-bearing activity.

  • Increased fluid intake (3000 to 4000 ml daily, cranberry or prune juice)

  • Hydration with isotonic saline infusion.

  • Bisphosphonates—gold standard.

  • Calcitonin.

Hypocalcemia

  • Low serum Ca levels caused by decreased production of PTH, multiple blood transfusions, alkalosis, increased calcium loss.

  • Manifestations: Positive Trousseau’s or Chvostek’s sign, laryngeal stridor, dysphagia, numbness and tingling around the mouth or in the extremities, dysrhythmias.

Tests for Hypocalcemia

  • Refer to the provided images demonstrating Trousseau's and Chvostek's signs.

Nursing and Interprofessional Management of Hypocalcemia

  • Treat cause.

  • Calcium and Vitamin D supplements.

  • IV calcium gluconate.

  • Rebreathe into paper bag.

  • Treat pain and anxiety to prevent hyperventilation-induced respiratory alkalosis.

Phosphate

  • Primary anion in ICF.

  • Essential to function of muscle, red blood cells, and nervous system.

  • Involved in acid-base buffering system, ATP production, cellular uptake of glucose, and metabolism of carbohydrates, proteins, and fats.

  • Serum levels controlled by parathyroid hormone.

  • Maintenance requires adequate renal functioning.

  • Reciprocal relationship with calcium.

Hyperphosphatemia

  • High serum PO_4^{3-} caused by acute kidney injury or CKD, excess intake of phosphate or vitamin D, hypoparathyroidism.

  • Manifestations: Tetany, muscle cramps, paresthesias, hypotension, dysrhythmias, seizures (hypocalcemia), calcified deposits in soft tissue such as joints, arteries, skin, kidneys, and corneas (cause organ dysfunction, notably renal failure).

  • Management: Identify and treat underlying cause, restrict intake of foods and fluids containing phosphorus, oral phosphate-binding agents, hemodialysis, volume expansion and forced diuresis, correct any hypocalcemia.

Hypophosphatemia

  • Low serum PO_4^{3-} caused by malnourishment/malabsorption, diarrhea, use of phosphate-binding antacids, inadequate replacement during parenteral nutrition.

  • Manifestations: CNS depression, muscle weakness and pain, respiratory and heart failure, rickets and osteomalacia.

  • Management: Increasing oral intake with dairy products, oral supplements, IV administration of sodium or potassium phosphate, monitor serum calcium and phosphorus levels every 6 to 12 hours.

Magnesium

  • Cofactor in enzyme for metabolism of carbohydrates.

  • Required for DNA and protein synthesis, blood glucose control, BP regulation.

  • Needed for ATP production.

  • Acts directly on myoneural junction.

  • Important for normal cardiac function.

  • 50% to 60% contained in bone, 30% in cells, only 1% in ECF.

  • Absorbed in GI tract, excreted by kidneys.

Hypermagnesemia

  • High serum Mg caused by increased intake of products containing magnesium when renal insufficiency or failure is present, excess IV magnesium administration.

  • Manifestations: Hypotension, facial flushing, lethargy, nausea and vomiting, impaired deep tendon reflexes, muscle paralysis, respiratory and cardiac arrest.

  • Management: Prevention first—stop magnesium-containing drugs and limit dietary intake of magnesium-containing foods, IV calcium gluconate if symptomatic, fluids and diuretics to promote urinary excretion, dialysis.

Hypomagnesemia

  • Low serum Mg caused by prolonged fasting or starvation, chronic alcoholism, fluid loss from GI tract, prolonged PN without supplementation, diuretics, proton-pump inhibitors, some antibiotics, hyperglycemic osmotic diuresis.

  • Manifestations: Resembles hypocalcemia, muscle cramps, tremors, hyperactive deep tendon reflexes, Chvostek’s and Trousseau’s signs, confusion, vertigo, seizures, dysrhythmias.

  • Management: Treat underlying cause, oral supplements, increase dietary intake, IV magnesium when severe.