Fluid and Electrolyte Imbalances: Practice Questions & Explanations

FLUID VOLUME EXCESS (FVE), also called hypervolemia or fluid overload, occurs when too much fluid is retained in the body. In HEART FAILURE, the failing heart cannot pump blood forward effectively; fluid backs up in the venous system and lungs.

Hallmark signs of fve: PERIPHERAL EDEMA — dependent edema (ankles/feet when upright, sacrum when supine); PULMONARY EDEMA — crackles (rales) at lung bases; dyspnea; orthopnea (difficulty breathing when lying flat); paroxysmal nocturnal dyspnea; WEIGHT GAIN — 1 kg ≈ 1 liter of fluid; 2 kg in 2 days is significant (daily weight is the MOST SENSITIVE early indicator of fluid retention); ELEVATED BLOOD PRESSURE — from increased circulating volume; JUGULAR VEIN DISTENSION (JVD) — at 45° head of bed elevation, visible jugular pulsation >2 cm above sternal angle indicates elevated central venous pressure; FULL, BOUNDING PULSE — from increased cardiac output/volume; INCREASED URINE OUTPUT (if kidneys are responding) — or decreased if kidneys are failing; S3 HEART SOUND ('gallop') — associated with heart failure. CONTRAST WITH FLUID VOLUME DEFICIT (FVD/hypovolemia): poor skin turgor; dry mucous membranes; decreased urine output with concentrated urine; tachycardia; decreased BP (orthostatic hypotension); flat neck veins; dizziness; weight loss; weak thready pulse. NURSING INTERVENTIONS for FVE:

Monitor: daily weight (same time, same scale, same clothing), I&O, vital signs, lung sounds, edema.

Diuretics: furosemide (Lasix) most common loop diuretic; FLUID RESTRICTION as ordered; low SODIUM DIET (sodium promotes water retention).

Position: semi-Fowler's or high-Fowler's for dyspnea.

Report: rapid weight gain (>1 kg/day), worsening dyspnea or crackles.

HYPERCALCEMIA is defined as serum calcium >10.5 mg/dL. Normal: 8.5-10.5 mg/dL. A level of 12.5 mg/dL is significantly elevated. CLINICAL MNEMONIC for hypercalcemia: 'BONES, GROANS, MOANS, AND STONES':

Bones: bone pain and pathological fractures — calcium is being leached from bones (especially in malignancy or hyperparathyroidism).

Groans: GI symptoms — nausea, vomiting, anorexia, CONSTIPATION (calcium decreases GI motility), abdominal pain.

Moans: neuropsychiatric — confusion, depression, psychosis, altered mental status, DECREASED DEEP TENDON REFLEXES (calcium stabilizes nerve membranes, reducing excitability), muscle weakness, fatigue, lethargy.

Stones: kidney stones (calcium oxalate or calcium phosphate) — polyuria, nephrolithiasis, nephrocalcinosis.

Cardiac effects: shortened QT interval on ECG (calcium shortens repolarization); dysrhythmias in severe cases.

Contrast with hypocalcemia: TETANY (muscle spasms, cramping); POSITIVE TROUSSEAU'S SIGN (carpal spasm when BP cuff inflated above systolic for 3 minutes); POSITIVE CHVOSTEK'S SIGN (facial muscle twitch when tapping the facial nerve anterior to the ear); PARESTHESIAS (perioral, fingertips); SEIZURES; INCREASED DEEP TENDON REFLEXES; PROLONGED QT INTERVAL on ECG.

Causes of hypercalcemia: MALIGNANCY (most common in hospitalized patients — bone metastases, PTH-related protein secretion); PRIMARY HYPERPARATHYROIDISM (most common cause overall in outpatients); vitamin D toxicity; prolonged immobilization; thiazide diuretics; sarcoidosis; milk-alkali syndrome.

Treatment: IV NORMAL SALINE (first-line — hydration promotes renal calcium excretion); FUROSEMIDE (after adequate hydration — promotes calciuresis); BISPHOSPHONATES (for malignancy-associated hypercalcemia); CALCITONIN (rapid but temporary); CORTICOSTEROIDS (for vitamin D-related causes, sarcoidosis); DIALYSIS (severe refractory cases).

Pn role: monitor for symptoms; hydration; fall risk (weakness, confusion); educate on adequate hydration; report severe symptoms or rapidly rising values.

FLUID VOLUME EXCESS RISK from IV fluid administration is a significant clinical concern, especially with rapid infusion rates. 2 LITERS IN 4 HOURS = 500 mL/hour — a moderately rapid rate; this is often appropriate in acute resuscitation but requires monitoring for fluid overload.

High-risk populations: Heart failure patients (already have fluid overload tendency; reduced cardiac output cannot accommodate extra volume); Renal insufficiency (kidneys cannot excrete excess fluid normally); Elderly patients (reduced cardiac reserve and renal function); Hypoalbuminemia (low oncotic pressure means more fluid shifts to interstitial space).

Monitoring for fluid overload:

Respiratory: Increasing respiratory rate; crackles (rales) in lung bases (fluid accumulating in alveoli); dyspnea; orthopnea.

Cardiovascular: Rising blood pressure; bounding pulse; jugular vein distension; S3 gallop on auscultation.

Peripheral: Dependent edema (ankles if upright, sacrum if supine); pitting edema.

Weight: Rapid weight gain (1 kg = approximately 1 liter of fluid).

Urine output: Should increase appropriately with fluid bolus; oliguria despite infusion suggests fluid is not being cleared.

Intervention if overload develops: Slow or stop the infusion; notify RN/provider; elevate HOB; administer supplemental oxygen; prepare for possible diuretic administration; continuous monitoring.

Fluid weight monitoring in heart failure:

Calculation: 1 kg = 1,000 mL of fluid; 1 lb ≈ 0.45 kg; 4 lbs ≈ 1.8 kg ≈ 1.8 liters of additional fluid.

Heart failure alert weight: Standard patient teaching: notify provider for weight gain of 2+ lbs in a day or 5+ lbs in a week; this patient has gained 4 lbs in 2 days — exceeds the alert threshold.

Assessment: Assess respiratory status (crackles, dyspnea, orthopnea — fluid moving to the lungs?); assess peripheral edema severity; review current medications (diuretics compliance?); check recent sodium intake.

Provider notification: This finding requires prompt provider communication; likely response: increase diuretic dose (furosemide adjustment); sodium restriction reinforcement; possibly additional monitoring or hospitalization if respiratory symptoms present.

Pn scope: Assess, document, notify RN/provider, implement ordered changes; daily weights are the most sensitive early indicator of fluid status changes.

HYPOKALEMIA from loop diuretics:

Normal potassium: 3.5-5.0 mEq/L.

Mild hypokalemia: 3.0-3.4 mEq/L (client's 3.1 mEq/L is mild).

Symptoms: Muscle weakness, cramps, fatigue (matching this client's complaints); SEVERE (<3.0): Potentially fatal cardiac dysrhythmias (PVCs, ventricular fibrillation), severe weakness.

Ecg changes: Flattened T waves, U waves, prolonged QU interval.

Intervention sequence: Notify provider with lab value and symptoms; HOLD furosemide (adding more diuretic increases potassium loss); REPLACE potassium: Oral KCl preferred when tolerated (less dangerous than IV); IV KCl if severe or oral not possible (NEVER IV push — causes cardiac arrest).

Dietary: Bananas, oranges, melons, potatoes, leafy greens, yogurt.

Monitoring: Repeat labs after replacement; cardiac monitoring if K+ <3.0; assess muscle weakness and ECG.

Renal: Ensure adequate renal function before aggressive replacement — hyperkalemia is also dangerous.

OLIGURIA (<30 mL/hr or <0.5 mL/kg/hr): This is a critical assessment finding.

Causes: Hypovolaemia (most common post-surgical — inadequate fluid replacement, haemorrhage); cardiac output reduction (heart failure, MI); renal causes (ATN, contrast nephropathy); obstruction (kinked catheter — check first); PRE-RENAL vs RENAL: Pre-renal oliguria responds to fluids; renal oliguria does not — distinguishing them guides treatment.

Immediate nursing actions: Check catheter for kinks, clots, or position issues (simple fix first); assess vital signs (hypotension + oliguria = volume depletion until proven otherwise); notify RN urgently — this requires medical assessment.

Anticipated orders: IV fluid bolus if pre-renal; renal panel, BMP; strict intake/output.

Pn scope: Assess, check equipment, NOTIFY RN IMMEDIATELY — do not wait; time-sensitive finding.

HYPONATRAEMIA (Na <135 mEq/L): SEVERE (<125 mEq/L): Neurological symptoms — confusion, nausea, headache, seizures, and if untreated, cerebral oedema, herniation, and death; 128 mEq/L with symptoms = URGENT;

Causes: SIADH (syndrome of inappropriate ADH secretion); heart failure; cirrhosis; excessive hypotonic IV fluids; psychogenic polydipsia.

Critical nursing action: Do NOT give free water or hypotonic fluids (water moves into cells and worsens cerebral oedema); Notify RN immediately; seizure precautions; TREATMENT (physician-ordered): Fluid restriction (most common); hypertonic saline (3% NaCl) for severe symptomatic cases — given only in ICU with strict monitoring; rate of correction must be controlled (correcting too fast causes osmotic demyelination syndrome).

Monitoring: Neurological status (confusion, seizure activity); vital signs; serum sodium levels; strict I&O; safety measures (fall precautions for confusion).

HYPONATREMIA (low sodium, <135 mEq/L): 122 mEq/L is significantly low.

Neurological effects dominate: Sodium imbalances primarily affect the brain because water shifts based on sodium concentration; LOW SODIUM = water moves INTO cells (including brain cells) = cerebral edema; SYMPTOMS by severity: Mild: headache, nausea, malaise; Moderate: confusion, lethargy, muscle weakness, disorientation; Severe (<120): seizures, coma, respiratory arrest, death.

Causes: SIADH, excessive water intake, diuretics, heart failure, vomiting/diarrhea with water replacement.

Treatment: Depends on cause and severity — fluid restriction (if dilutional), careful sodium replacement (hypertonic saline for severe symptomatic cases — corrected SLOWLY to avoid osmotic demyelination syndrome).

Safety: Seizure precautions for severe hyponatremia; LPN role: monitor neuro status, report changes, implement safety measures.

IV POTASSIUM SAFETY — A HIGH-ALERT MEDICATION: KCl is irritating to veins and dangerous if administered incorrectly. BURNING at the site: Slow or stop the infusion; assess for infiltration; KCl is a vein irritant — slower rates and greater dilution reduce burning; consider a central line for higher concentrations;

Never IV push: Concentrated IV potassium push causes immediate fatal cardiac arrest (cardioplegia) — KCl must ALWAYS be diluted and infused slowly.

Administration rules: Maximum peripheral concentration and rate per protocol (typically not exceeding 10 mEq/hour peripherally without cardiac monitoring); always use an infusion pump; never bolus.

Cardiac monitoring: For higher rates or concentrations.

Hyperkalemia risk: Too much/too fast potassium causes hyperkalemia → peaked T waves, widened QRS, fatal dysrhythmias; ASSESS renal function before administration (impaired kidneys can't excrete potassium); LPN role: monitor IV site, infusion rate, never administer KCl IV push, report burning or cardiac symptoms.