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 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.
Intracellular Fluid (ICF): 28 L
Extracellular Fluid (ECF)
Plasma: 3 L
Interstitial Fluid (IF): 10 L
1 L of water weighs 2.2 pounds (1 kg).
Body weight change is a good indicator of overall fluid volume loss or gain.
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.
ICF
Prevalent cation: K^+ potassium
Prevalent anion: PO_4^{3-} phos
ECF
Prevalent cation: Na^+ ssodium
Prevalent anion: Cl^- chloride
Refer to the provided diagrams for specific concentrations of cations and anions in plasma and intracellular fluid (ICF).
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.
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).
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 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.
Determined by:
Capillary hydrostatic pressure
Plasma oncotic pressure
Interstitial hydrostatic pressure
Interstitial oncotic pressure
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
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.
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).
Renal perfusion:
↓Renal perfusion → ↑ Renin secretion → ↑ Plasma angiotensin II → ↑ Aldosterone secretion
Other factors:
Stress, physical trauma, ↑ Serum K^+, ↓ Serum Na^+, ↑ ACTH
Stress → Hypothalamus (CRH) → Anterior pituitary (↑ ACTH secretion) + Posterior pituitary (↑ ADH secretion).
Adrenal cortex (↑ Aldosterone, ↑ Cortisol) → Kidney (↑ Na^+ reabsorption, ↑ K^+ excretion, ↑ H_2O reabsorption)
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.
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 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).
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
Refer to the provided images for assessing skin turgor.
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.
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.
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.
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^+)
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
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.
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.
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.
Tall, peaked T wave.
Prolonged PR interval.
Widened QRS.
Depressed ST segment.
Wide, flat P wave.
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.
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.
Slightly prolonged PR interval.
ST depression.
Slightly peaked P wave.
Shallow T wave.
Prominent U wave.
Decreased R wave amplitude.
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.
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.
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.
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.
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.
Refer to the provided images demonstrating Trousseau's and Chvostek's signs.
Treat cause.
Calcium and Vitamin D supplements.
IV calcium gluconate.
Rebreathe into paper bag.
Treat pain and anxiety to prevent hyperventilation-induced respiratory alkalosis.
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.
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.
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.
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.
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.
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.