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Chapter 1-7 Fluids and Electrolytes: Practice Flashcards

Hypovolemia and Dehydration

  • Distinct terminology
    • Hypovolemia: extracellular fluid (ECF) deficit with decreased circulating blood volume.
    • Dehydration: fluid loss leading to increased solute concentration in blood.
    • Extracellular fluid is the fluid outside cells, including the fluid in the vasculature (the “pipes”).
    • These conditions often occur together but may occur separately.
  • Etiology (cause) of hypovolemia
    • GI losses (vomiting, diarrhea) – common cause
    • Renal losses (polyuria, diuretics, diabetes insipidus can affect urine output)
    • Skin losses (sweating, burns)
    • Third spacing and hemorrhage are usually pathologic
  • Third spacing and hemorrhage
    • Third spacing: interstitial fluid trapped in spaces where it’s not in cells or vasculature
    • Hemorrhage: actual loss of blood volume, externally or internally
  • Clinical cues and vital signs (early warning signs)
    • Vital sign changes reflect internal fluid deficit
    • Weak peripheral pulses, delayed capillary refill, decreased urine output, concentrated urine
    • Low blood pressure due to reduced perfusion
  • Lab indicators and pathophysiology
    • Hemoconcentration: higher proportion of red blood cells relative to plasma when fluid is depleted
    • BUN and creatinine rise with reduced kidney perfusion/function
    • Increased serum osmolality, especially sodium-related shifts
    • Urine specific gravity increases (concentrated urine)
    • Key electrolyte focus: sodium is the major extracellular cation
  • Priorities in assessment and management
    • Assess: vital signs, mental status, urine output
    • Restore volume with appropriate fluids; monitor before, during, and after repletion
    • Educate to prevent recurrence
  • Pharmacologic management (fluids as drugs)
    • Isotonic fluids for volume replacement when the goal is to restore intravascular volume
    • Isotonic fluids help avoid creating a new osmotic gradient across cell membranes
    • Colloids (e.g., albumin) may be needed if hypoalbuminemia prevents retention of infused fluid (fluid will leak back out otherwise)
    • Crystalloids vs colloids: crystalloids are first-line; colloids used when intravascular volume expansion is not sustained due to low oncotic pressure
    • Vasopressors are reserved for later consideration if fluid resuscitation fails to restore adequate pressure (not needed as a first-line action)
    • If electrolyte abnormalities coexist, address and correct them
  • Conceptual sequence in a hypovolemic patient
    • First: restore circulating volume with fluids (crystalloids), monitor response
    • If inadequate response: consider colloids (e.g., albumin) to raise oncotic pressure
    • If volume status remains uncorrected or hypotension persists: escalate to critically oriented interventions (vasopressors, ICU care) and consider advanced resuscitation strategies
  • Question example and reasoning (critical thinking in nursing)
    • If hypovolemic, what clinical finding would you expect?
    • Low blood pressure (hypotension) due to reduced circulating volume
    • Weak, non-bounding peripheral pulses; not strong; central pulses may be weak
    • Urine specific gravity would be high (concentrated urine), not low
    • Hematocrit would be increased (hemoconcentration), not decreased
  • Practical clinical tips mentioned in the lecture
    • Emphasized that fluid is a pharmacologic agent in this context
    • Connect vital signs to the underlying pathophysiology (e.g., low BP with poor perfusion)
    • The instructor notes that lecture notes contain detailed thought processes for problem-solving approaches

Hypervolemia (Fluid Overload)

  • Definition and causes
    • Excess extracellular fluid with overall increased circulating volume
    • Etiologies include excessive IV fluid administration and organ dysfunction that impairs fluid handling (heart, kidneys, liver)
    • Liver disease can raise fluid retention via reduced albumin production; high sodium diet can promote water retention
  • Pathophysiology and consequences
    • Hydrostatic pressure rises, promoting fluid movement into interstitial spaces (edema) and third spacing
    • Hemodilution occurs as the intravascular plasma portion becomes diluted
    • May dilute serum sodium; overall body fluids increase; hematocrit decreases (hemodilution)
  • Clinical manifestations
    • Signs of high circulating volume: hypertension, bounding pulses, edema, weight gain
    • Respiratory symptoms: crackles in the lungs, dyspnea, potential hypoxia
    • Daily weights and strict input/output monitoring are key
  • Lab and monitoring implications
    • Hematocrit may decrease due to hemodilution
    • Serum sodium may be diluted if fluid retention is excessive
    • Watch for signs of pulmonary edema and electrolyte shifts
  • Nursing priorities and management plan
    • Prioritize respiratory status: ensure adequate oxygenation and assess work of breathing
    • Consider diuresis to remove excess fluid (will be covered in module on diuretics)
    • Elevate edematous limbs to improve venous return and reduce edema burden in the lungs
    • Monitor fluid balance: daily weights, intake, and output
    • Fluid and sodium restriction as appropriate
    • If edema persists or severe symptoms occur, escalate care (intensive monitoring, diuresis, and possibly ACE inhibitors/ARMs to reduce afterload and promote fluid removal)
    • In severe cases of fluid overload with organ failure or life-threatening edema, dialysis may be required
  • Case example and reasoning
    • Heart failure patient with a rapid 3 kg (≈6 lb) weight gain in 2 days and crackles in the lungs
    • Nursing priority: address oxygenation first (e.g., ensure adequate oxygenation/SpO2) before other interventions
    • Subsequent steps include diuresis, fluid/sodium restriction, and close monitoring of vital signs and respiratory status
  • Concept of third-spacing management in hypervolemia
    • If fluid is third-spaced (not readily re-entering vasculature), diuretics alone won’t be effective until fluid is pulled back into intravascular space
    • Use hypertonic solutions or colloids (e.g., hypertonic saline, albumin) to draw interstitial fluid back into the intravascular space, enabling diuresis to remove the excess
  • Dialysis and advanced therapies
    • Dialysis may be necessary in life-threatening cases where fluid is not controllable by diuretics or when renal failure is present
    • ICU-level care may be required for continuous monitoring and interventions
  • Quick clinical takeaway
    • Fluid overload requires a staged approach: ensure airway/oxygenation, reduce volume via diuresis and fluid/sodium restriction, and escalate care if needed
    • Use of hypertonic solutions or colloids to mobilize interstitial fluid back into the circulatory space may be necessary before diuresis

Electrolyte Imbalances: Core Concepts and Regulation

  • Core electrolytes to memorize (highest-yield)
    • Potassium (K+): intracellular primary cation; crucial for cardiac rhythm and neuromuscular function
    • Sodium (Na+): extracellular primary cation; major determinant of osmolality and fluid shifts
    • Calcium (Ca2+): essential for muscle contraction, neuromuscular function, bone health; present in both intra- and extracellular compartments
    • Magnesium (Mg2+): intracellular cation; influences neuromuscular excitability and reflexes; interacts with calcium and potassium
    • Optional: phosphate and chloride/bicarbonate also important in broader physiology
  • Regional distribution overview
    • Potassium: predominantly inside cells
    • Sodium: predominantly outside cells
    • Magnesium and phosphate: more inside cells
    • Chloride and bicarbonate: more outside cells
    • Calcium: present both inside and outside cells; extracellular calcium important for signaling and contraction
  • Regulatory mechanisms
    • Intake vs. renal excretion determine overall balance
    • Hormonal regulation: aldosterone, parathyroid hormone (PTH), calcitonin regulate sodium and calcium
    • Insulin drives potassium from extracellular fluid into cells (acts as a pump-like regulator)
    • ATP-powered pumps (e.g., Na+/K+-ATPase) maintain resting membrane potential and ion gradients
  • Important quantitative reference points (ranges to memorize)
    • Sodium: 135-145 ext{ mEq/L}
    • Potassium: tight control around 3.55 ext{ mEq/L} (lower limit for safe cardiac conduction; clinically significant shifts occur with small changes)
    • Magnesium: normal range roughly around 1.5-2.5 ext{ mg/dL} (precise ranges vary by lab; small deviations matter clinically)
    • Calcium: normal serum range roughly 8.5-10.5 ext{ mg/dL} (value can vary by assay)
  • Sodium abnormalities
    • Hyponatremia (Na+ too low): causes include GI losses, excess ADH/SIADH, water intoxication
    • Neurologic manifestations: confusion, seizures, weakness
    • Management cues:
    • Mild hyponatremia: consider oral salt tablets or dietary adjustments
    • Severe hyponatremia: may require hypertonic saline (e.g., 3% NaCl) under careful monitoring
    • ADH antagonists can help SIADH by reducing water reabsorption in kidney (e.g., vasopressin antagonists) – not deeply covered here
    • Diabetes insipidus represents the opposite (excess water loss); treat with fluids and measures to maintain ADH activity
    • When correcting hyponatremia, rate of correction matters to avoid osmotherapeutic complications
  • Potassium (K+) disorders and ECG risk
    • Hypokalemia: can cause weakness, arrhythmias; ECG changes include flattened or low T waves
    • Hyperkalemia: can cause dangerous arrhythmias; ECG changes include peaked T waves
    • Potassium repletion: administer potassium chloride as needed; monitor closely on cardiac monitor
    • Potassium-sparing vs potassium-wasting diuretics: strategies depend on K+ status
    • Severe hyperkalemia management sequence (stepwise):
    • 1) Calcium gluconate to stabilize cardiac membranes
    • 2) Insulin + glucose to drive K+ into cells (glucose to prevent hypoglycemia)
    • 3) Cation-exchange resin (K-exalate) to bind potassium in GI tract and eliminate it
    • 4) Dialysis if refractory or in renal failure
  • Calcium (Ca2+) disorders
    • Hypocalcemia commonly due to hormonal imbalances (e.g., hypoparathyroidism) and vitamin D deficiency
    • Tetany: muscle spasms due to low calcium; signs of neuromuscular irritability
    • Symptoms can include muscle cramps, tingling, convulsions, and arrhythmias in severe cases
    • Management themes: address underlying hormonal issues, calcium supplementation as needed, monitor for neuromuscular symptoms
  • Magnesium (Mg2+) disorders
    • Magnesium imbalance affects reflexes and neuromuscular excitability; tremors and seizures can be linked to Mg2+ status
    • Magnesium interacts with calcium and potassium in neuromuscular function
  • Insulin and potassium shift
    • Insulin drives potassium from extracellular fluid into cells; this effect is independent of blood glucose handling and can precipitate hypokalemia if not carefully monitored
    • In potassium repletion or redistribution strategies, ECG monitoring is essential due to potential cardiac effects
  • Practical application and clinical reasoning
    • Always monitor cardiac status (ECG) when addressing potassium disturbances due to the heart’s sensitivity to K+ changes
    • Distinguish neurologic symptoms caused by sodium vs. calcium vs. magnesium disturbances; overlap exists, but patterns help with interpretation
    • When treating hyponatremia, consider the patient’s fluid status; hyponatremia with edema may require careful, slower correction to avoid osmotic demyelination
  • Summary of key relationships and clinical implications
    • Fluid balance and electrolytes are tightly linked: shifts in fluid compartments affect electrolyte concentrations and vice versa
    • Management often requires staged, carefully monitored interventions to restore balance without causing iatrogenic harm
    • A patient on critical electrolyte disturbances should generally be on continuous ECG monitoring due to the risk of arrhythmias and the heart’s sensitivity to even small shifts

Quick reference: Formulas and practical notes

  • Isotonic fluid goal for volume replacement in hypovolemia: avoid creating osmotic gradients across cell membranes; use fluids like 0.9% NaCl or lactated Ringer's
  • Half-normal saline (0.45% NaCl): used to slowly dilute plasma when appropriate and to avoid rapid shifts in serum osmolality
  • Hypertonic saline (e.g., 3% NaCl): used in severe hyponatremia or specific hyperosmolar states to pull water from cells and correct sodium deficit
  • Albumin (colloid): used to expand intravascular volume when hypoalbuminemia prevents effective fluid retention
  • Potassium handling reminders
    • Normal K+ range is tightly regulated; clinically significant shifts can cause arrhythmias
    • Potassium chloride is used to correct hypokalemia; potassium-sparing diuretics may be used to minimize K+ losses in certain contexts
    • Severe hyperkalemia management sequence emphasizes calcium stabilization first, then potassium redistribution and removal
  • Sodium management reminders
    • SIADH: excess ADH leading to hyponatremia; consider ADH antagonists when appropriate
    • Diabetes insipidus: opposite problem with hypernatremia risk; manage with free water and ADH replacement as appropriate
  • Calcium and neuromuscular function
    • Tetany is a hallmark sign of hypocalcemia; management centers on correcting calcium and addressing underlying hormonal issues
  • Magnesium and neuromuscular function
    • Mg2+ status influences reflexes and tremors; monitor closely in patients with suspected magnesium disturbances

Connections to broader concepts

  • Links to pharmacology: fluids are considered drugs with therapeutic intent; choosing crystalloids vs colloids, and deciding when vasopressors or diuretics are warranted, reflects pharmacologic decision-making
  • Ethical/practical implications: the rate of correction for electrolyte disturbances must balance efficacy with risk of complications (e.g., osmotic demyelination with overly rapid sodium correction)
  • Real-world relevance: daily weights, intake/output logs, and careful monitoring are foundational to prevent progression from compensable to decompensated states
  • Foundational physiology connections: diffusion and osmosis principles explain fluid shifts; ATP-powered pumps and hormonal regulation (aldosterone, PTH, calcitonin, ADH) explain electrolyte handling and distribution