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