Fluids and Electrolytes

Total body water

60% of adult body weight (varies by age, gender, and adipose tissue)

Intracellular fluid

• 2/3 of body water (approx. 40% of body weight)

• Primary cation: Potassium

• Primary anion: Phosphate

Extracellular fluid

• 1/3 of body water (approx. 20% of body weight)

• Primary cation: Sodium

• Primary anion: Chloride

Intravascular

• Type of ECF

• Plasma (5% of body weight)

Interstitial

• Type of ECF

• Fluid surrounding cells/lymph (15% of body weight)

Transcellular

• Type of ECF

• Cerebrospinal, pericardial, synovial, pleural fluids (approx. 1%)

Osmosis

Movement of water across a semipermeable membrane from low solute concentration to high solute concentration

Diffusion

Movement of solutes from high concentration to low concentration

Filtration

Movement of water and solutes from high hydrostatic pressure to low pressure (e.g. arterial end of capillary bed)

Active transport

Movement against a concentration gradient requiring ATP (e.g. Sodium-potassium ATPase pump)

Isotonic solution

• 275-295 mOsm/L

• Same osmolality as plasma

• No net fluid shift

• e.g. 0.9% NaCl, Lactated Ringer’s, D5W in the bag

Hypotonic solution

• <275 mOsm/L

• Lower osmolality than plasma

• Drives fluid into cells leading to cellular swelling

• e.g. 0.45% NaCl

Hypertonic solution

• >295 mOsm/L

• Higher osmolality than plasma

• Pulls fluid out of cells leading to cellular shrinkage

• e.g. 3% NaCl, D5NS, D10W

Isotonic solution

• Osmolality vs Plasma: Equal

• Cell effect: No volume change

• Clinical indication: Fluid resuscitation, intravascular expansion

Hypotonic solution

• Osmolality vs Plasma: Lower

• Cell effect: Swells (fluid shift ICF)

• Clinical indication: Cellular dehydration (e.g. DKA)

Hypertonic

• Osmolality vs Plasma: Higher

• Cell effect: Shrinks (fluid shifts ECF)

• Clinical indication: Severe hyponatremia, cerebral edema

isotonic; hypotonic

D5W is _________, but it becomes __________ in the body once glucose is metabolized by the cells.

D5W

• Cell swelling: Do not use in patients with increased intracranial pressure or head trauma, as fluid shifting into cells can worsen brain swelling

• Not for resuscitation: It does not stay in the blood vessels long enough to treat acute blood loss or severe low blood pressure

• Free water supply: Used to treat cellular dehydration and high sodium levels

Kidneys (primary regulator)

• Filter approximately 180 L of plasma a day

• Produce 1-2 L of urine/day

• Regulate ECF volume, electrolyte levels, and pH

Heart and blood vessels

Pumping action maintains renal perfusion needed for filtration

Lungs

• Exhale approx. 300-400 ml/day (insensible loss)

• Maintain acid-base balance via CO2 excretion

Pituitary and hypothalamus

Synthesize and release antidiuretic hormone (ADH) to retain water

Adrenal cortex

Releases aldosterone in response to low serum sodium or elevated potassium, causing sodium and water retention and potassium excretion

Sensible loss

• Loss that is measurable

• e.g. Urine = 30 ml/hr minimum, bowel

Insensible loss

• Loss that is non-measurable

• e.g. Skin evaporation, lungs = approx. 500-1000 ml/day

Gerontologic

These people have reduced total body water (45-50%), diminished thirst sensation, reduced renal concentration ability, and decreased renin/aldosterone levels leading to high risk for rapid dehydration.

• GI loss (vomiting, diarrhea, NGT suctioning)

• Excessive sweating

• Hemorrhage

• Renal losses (diuretics, Diabetes Insipidus)

• Third-space fluid shifts (burns, peritonitis, intestinal obstruction)

Etiology of fluid volume deficit/hypovolemia

Loss of ECF volume exceeds intake. Equal loss of solutes and water leads to isotonic fluid deficit, reducing intravascular volume and organ perfusion.

Pathophysiology of fluid volume deficit/hypovolemia

• Acute weight loss (≥ 2% mild; ≥ 5% moderation; ≥ 8% severe)

• Decreased skin turgor (tenting), dry mucous membranes

• Oliguria (<30 ml/hr) or concentrated urine

• Postural/orthostatic hypotension, weak and rapid thready pulse, flattened neck veins

• Increased body temperature (unless in shock)

FVD signs and symptoms:

• Elevated BUN out of proportion to creatinine (BUN:Cr ratio > 20:1)

• Increased hematocrit (hemoconcentration)

• Increased urine specific gravity (> 1.030) and urine osmolality

Diagnostic findings in FVD

Oral dehydration (isotonic fluids/water)

Medical management for mild FVD

Isotonic fluids (0.9% NS or LR) to restore vascular volume, followed by hypotonic solutions (0.45% NaCl) once normotensive

Medical management for severe FVD

• Monitor I&O: Measure hourly if unstable; alert provider if urine output is <0.5 ml/kg/hr

• Daily weights: Same scale, same time, same clothing (1 kg weight loss = 1L fluid loss)

• Vital signs: Check for orthostatic changes (drop in SBP > 20 mmHg upon standing)

• Safety: Fall precautions due to orthostatic hypotension

Nursing interventions for FVD

• Heart failure

• Renal failure

• Cirrhosis of the liver

• Excessive IV fluid administration (0.9% NaCl)

• Hyperaldosteronism

Etiology of fluid volume excess/hypervolemia

Isotonic expansion of ECF due to abnormal retention of water and sodium in roughly equal proportions. Serum sodium remains near normal, but total body sodium and water expand.

Pathophysiology of fluid volume excess/hypervolemia

• Peripheral edema (pitting) and sacral edema in bedridden patients

• Distended neck veins (Jugular Venous Distention/JVD)

• Crackles (rales) in lung bases, dyspnea, shortness of breath, orthopnea, cough

• Bounding rapid pulse, elevated BP, elevated Central Venous Pressure (CVP)

• Rapid weight gain over short duration

Signs and symptoms of FVE

• Decreased hematocrit and hemoglobin (hemodilution)

• Decreased BUN (hemodilution)

• Low serum osmolality

• Chest x-ray: pulmonary vascular congestion, pleural effusion

Diagnostic findings in FVE

• Loop diuretics (Furosemide/Lasix)

• Thiazide diuretics (Hydrochlorothazide)

Pharmacological medical management of FVE

• Sodium restriction (1-2 g/day)

• Fluid resuscitation if severe

Dietary medical management of FVE

Renal replacement therapy (Hemodialysis/peritoneal dialysis)

Medical management for severe renal impairment in FVE

• Assess breath sounds q2-4h for worsening pulmonary edema

• Position in semi-Fowler’s or high-Fowler’s to promote lung expansion

• Monitor I&O, daily weight, and strict adherence to fluid resuscitations

• Turn and reposition q2h to protect edematous tissue from pressure injury

Nursing interventions for FVE

Fluid volume deficit

• BP: Hypotension/orthostatic

• PR/Quality: Tachycardia/weak, thready

• Jugular veins: Flat

• Respirations: Normal or rapid

• Hematocrit/BUN: Elevated (hemoconcentration)

• Primary risk: Hypovolemic shock

Fluid volume excess

• BP: Hypertension

• PR/Quality: Tachycardia/bounding

• Jugular veins: Distended (JVD)

• Respirations: Dyspnea, crackles, tachypnea

• Hematocrit/BUN: Decreased (hemodilution)

• Primary risk: Pulmonary edema and heart failure

Daily weight (1 kg = 2.2. lbs = 1,000 ml)

What is the single most accurate indicator of fluid status?

Fluid challenge test

• Used to distinguish pre-renal azotemia (dehydration) from intrinsic renal failure

• Infuse 100-200 ml normal saline over 15 minutes

• Increased urine output confirms hypovolemia

Third-spacing alert

• Fluid moves into non-functional spaces (ascites, burn blisters)

• The patient shows signs of severe hypovolemia despite high scale weight

135-145 mEq/L

Normal range of sodium

3.5-5.0 mEq/L

Normal range of potassium

• 8.5-10.5 mg/dl (total)

• 4.5 - 5.1 mg/dl (ionized)

Normal range of calcium

Total calcium

Measures all forms of calcium in the blood

Ionized calcium

Measures only the free, biologically active form of calcium

1.3-2.3 mEq/l

Normal range of magnesium

2.5-4.5 mg/dl

Normal range of phosphorus

98-106 mEq/l

Normal range of chloride

• Hyperparathyroidism

• Bone malignancies/metastasis

• Prolonged immobilization

• Thiazide diuretics

Etiology of hypercalcemia:

Elevated calcium reduces neuromuscular excitability, slowing cardiac, smooth, and skeletal muscle response

Pathophysiology of hypercalcemia

• Bones: bones pain, pathologic fractures

• Stones: renal calculi (kidney stones)

• Groans: constipation, anorexia, nausea, vomiting, and paralytic ileus

• Psychiatric overtones: confusion, lethargy, coma, depression

• Cardiac: shortened QT interval, dysrhythmias

Signs and symptoms of hypercalcemia

• SADH

• Heart failure

• Excessive administration of D5W IV

• Vomiting

• Diarrhea

• Diaphoresis

• Thiazide diuretics

Etiology of hyponatremia:

Low ECF sodium content lowers serum osmolality. Water shifts from ECF into ICF, causing cells (especially brain cells) to swell.

Pathophysiology of hyponatremia:

• Neurological: Headache, confusion, lethargy, altered mental status, papilledema, seizures, coma

• Musculoskeletal: Muscle cramps, weakness

• GI: Anorexia, nausea, vomiting, abdominal cramps

Signs and symptoms of hyponatremia:

• Serum sodium < 135 mEq/L

• Serum osmolality < 280 mOsm/kg

Diagnostics for hyponatremia

Water restriction (primary therapy)

Medical management for hyponatremia when euvolemic or hypervolemic

0.9% normal saline IV

Medical management for hyponatremia when hypovolemic

Small doses of 3% hypertonic saline via central line

Medical management for hyponatremia when severe or symptomatic (< 120 mEq/L with seizures)

• Seizure precautions (pad side rails, suction ready)

• Monitor neurological status q1-2h

Nursing interventions for hyponatremia

Osmotic demyelination syndrome (Central pontine myelinolysis)

This occurs due to rapid correction of sodium (> 8-12 mEq/L in 24 hours) which causes irreversible neurological damage/paralysis. Correct serum sodium slowly!

• Diabetes insipidus

• Hypertonic tube feedings without adequate free water

• Heat stroke

• Hyperventilation

• Water deprivation

Etiology of hypernatremia

High ECF sodium increases ECF osmolality. Water shifts from ICF into ECF, causing cellular dehydration and neuronal shrinkage.

Pathophysiology of hypernatremia

• Neurological: Restlessness, agitation, irritability, hallucinations, hyperreflexia, seizures

• Physical: Intense thirst, dry, sticky mucous membranes, flushed, dry skin, swollen, red tongue

Signs and symptoms of hypernatremia

• Loop and thiazide diuretics (Furosemide)

• GI losses (vomiting, diarrhea, NGT suctioning)

• Metabolic alkalosis

• Hyperaldosteronism

• Persistent insulin administration

Etiology of hypokalemia

Low extracellular potassium impairs membrane resting potential, causing hyperexcitability followed by refractory unresponsiveness in neuromuscular and cardiac tissues

Pathophysiology of hypokalemia

• Cardiac: Dysrhythmias, increased sensitivity to Digitalis toxicity

• ECG changes: Flattened/inverted T waves, ST depression, prominent U waves

• Neuromuscular: Muscle weakness, leg cramps, fatigue, paresthesias

• GI: Decreased motility, constipation, paralytic ileus

Signs and symptoms of hypokalemia

• Never IV push, IV bolus, or IM

• Must be diluted

• Infusion pump only (max rate: 10-20 mEq/hr)

• Assess renal output before giving: Urine output must be at least 30 ml/hr (“No pee = No K+)

How is potassium administered?

• Oral potassium replacement (take with food to avoid GI upset)

• IV potassium chloride replacement for severe deficiency

Medical management for hypokalemia

• Acute/chronic renal failure

• Addison’s disease

• Potassium-sparing diuretics (spironolactone)

• Tissue trauma/burns (cell lysis)

• Metabolic acidosis

Etiology of hyperkalemia

High ECF potassium partially depolarizes cell membranes, altering cardiac conduction speed and muscle contractility

Pathophysiology of hyperkalemia

• Cardiac: Bradycardia, heart block, ventricular fibrillation, cardiac arrest

• ECG changes: Tall, peaked T waves, wide QRS complex, prolonged PR interval, flat P wave

• Neuromuscular: Paresthesias, muscle twitching → flaccid muscle paralysis

• GI: Hyperactive bowel sounds, abdominal cramping, diarrhea

Signs and symptoms of hyperkalemia

IV calcium gluconate

• Hyperkalemia emergency medical management

• Antagonizes cardiac membrane excitability (protects heart)

• Speed of onset is 1-3 minutes (immediate)

IV regular insulin + D50

• Hyperkalemia emergency medical management

• Shifts potassium into cells

• Speed of onset is 15-30 minutes

Inhaled albuterol

• Hyperkalemia emergency medical management

• Also shifts potassium into cells

• Speed of onset is also 15-30 minutes

Sodium bicarbonate

• Hyperkalemia emergency medical management

• Alkalinizes plasma, shifting potassium into cells

• Speed of onset is 15-30 minutes

Sodium polystyrene sulfonate (Kayexalate)

• Hyperkalemia emergency medical management

• Binds potassium in bowel for fecal excretion

• Speed of onset is hours (slow)

Loop diuretics/dialysis

• Hyperkalemia emergency medical management

• Removes potassium from the body

• Speed of onset is variable/definitive

• Hypoparathyroidism (accidental removal during thyroidectomy)

• Vitamin D deficiency

• Acute pancreatitis

• Massive blood transfusions (citrate toxicity)

• Chronic kidney disease

Etiology of hypocalcemia

Low serum calcium increases nerve cell membrane permeability to sodium, causing neuromuscular hyperexcitability and involuntary muscle contractions.

Pathophysiology of hypocalcemia

• Chvostek’s sign

• Trousseau’s sign

• Tetany, circumoral paresthesia (tingling lips/fingers), laryngospasm

• ECG: Prolonged QT interval → risk for Torsades de Pointes

Signs and symptoms of hypocalcemia

Chvostek’s sign

Facial twitching when tapping the facial nerve (CN VII) (anterior to ear)

Trousseau’s sign

Occluding brachial artery with BP cuff → ischemia-induced carpopedal spasm (flexion of wrist/thumb)

Tracheostomy tray and IV calcium gluconate

In post-thyroidectomy nursing care, what should you keep at the bedside due to immediate risk of severe hypocalcemia and life-threatening laryngospasm?

• Chronic alcoholism

• Malbasorption syndromes (Celiac, Crohn’s)

• Aminoglycoside antibiotics

• Propton pump inhibitors

• Diarrhea

Etiology of hypomagnesemia

Magnesium controls the sodium-potassium pump and cellular energy (ATP). Deficiency leads to increased neuromuscular hyperexcitability (similar to hypocalcemia)

Pathophysiology of hypomagnesemia

• Hyperactive deep tendon reflexes (DTRs, +3/+4)

• Positive Chvostek’s and Trosseau’s signs

• Neuromuscular: Tremors, tetany, seizures, altered mood

• Cardiac: ECG shows prolonged PR/QT intervals, Torsades de Pointes (polymorphic VTach)

Signs and symptoms of hypomagnesemia

Hyperkalemia

Identify the electrolyte imbalance based on the ECG:

• Peaked T wave

• Wide QRS complex

• Flat P wave

Hypokalemia

Identify the electrolyte imbalance based on the ECG:

• Flat/inverted T wave

• ST depression

• U wave

Hypercalcemia

Identify the electrolyte imbalance based on the ECG:

• Shortened ST segment

• Shortened QT interval

• Wide T wave

Hypocalcemia

Identify the electrolyte imbalance based on the ECG:

• Prolonged ST segment

• Prolonged QT interval

Hypermagnesemia

Identify the electrolyte imbalance based on the ECG:

• Prolonged PR interval

• Widened QRS complex

Hypomagnesemia

Identify the electrolyte imbalance based on the ECG:

• Tall T wave

• ST depressed

• Prolonged QT interval

• Renal failure

• Excessive administration of magnesium during eclampsia treatment

• Overuse of Mg-containing antacids/laxatives (milk of magnesia)

Etiology of hypermagnesemia

High magnesium depresses the central nervous system and neuromuscular junction, blocking acetylcholine release

Pathophysiology of hypermagnesemia