The Cellular Environment: Fluids and Electrolytes - Vocabulary Flashcards (Video Notes)

Key Concepts

  • The cellular environment focuses on fluids and electrolytes and how they are regulated in the body.
  • Major goals include understanding regulation of fluid/electrolyte balance, fluid compartments, movement of fluids, and common imbalances and their clinical implications.
  • Key regulators include thirst, antidiuretic hormone (ADH/vasopressin), the renin–angiotensin–aldosterone system (RAAS), and natriuretic peptides.

Fluid Compartments and Body Fluids

  • Total body water (TBW) is distributed across compartments:
    • Intracellular fluid (ICF): inside cells
    • Extracellular fluid (ECF): outside cells, includes plasma (intravascular) and interstitial fluid
    • Specific fluids mentioned: cerebrospinal fluid (CSF)
  • Fluid balance concepts:
    • Filtration: movement of fluid out of capillaries into interstitial space
    • Reabsorption: movement of fluid from interstitial space back into capillaries
  • Visual distribution cues (described schematically):
    • Intracellular water vs extracellular (plasma) water vs extracellular (interstitial) water

Aging and Distribution of Body Fluids

  • TBW percentages by life stage:
    • Newborn: 70 ext{–}80 ext{%} of body weight
    • Childhood: 60 ext{–}65 ext{%} of body weight
    • Adults: 50 ext{–}60 ext{%} of body weight
    • Older adults: percent declines with age
  • Gender difference: Men tend to have a greater percentage of body water than women due to more muscle mass

Fluid Imbalances: Volume Deficit (Hypovolemia)

  • Definition: abnormal loss of body fluids, inadequate fluid intake, or plasma to interstitial fluid shift
  • Cellular consequence: cells become dehydrated
  • Key consideration: correcting volume deficit too quickly can cause undesirable fluid shifts

Fluid Imbalances: Volume Excess (Hypervolemia)

  • Definition: excess fluid intake, abnormal fluid retention, or interstitial-to-plasma fluid shift
  • Common causes: kidney dysfunction, cardiac dysfunction

Overhydration and Clinical Manifestations

  • Overall picture: fluid volume excess with signs of shifting osmolality and organ system effects
  • Brain, heart, lungs, abdomen are high-risk areas when vascular osmotic/oncotic pressure is low or fluid shifts occur
  • Clinical manifestations of fluid overload (illustrative features):
    • Neurologic: altered level of consciousness, confusion, seizures
    • Respiratory: pulmonary congestion
    • Cardiovascular: bounding pulse, increased BP, JVD, S3, tachycardia
    • Gastrointestinal: anorexia, nausea
  • Lab indicators often include: changes in urine concentration (e.g., urine specific gravity), BUN, and hematocrit changes due to dilution
  • Visual: edema can present as dependent edema and generalized swelling

Osmolarity and Osmolality

  • Osmolarity: concentration of molecules per liter of solution; often used for fluids outside the body
  • Osmolality: concentration of molecules per kilogram of water; often used for describing fluids inside the body

Water Movement Between ICF and ECF

  • Water movement is primarily driven by osmotic forces between ICF and ECF
  • Filtration vs. reabsorption in capillaries:
    • Filtration: fluid moves out of capillaries into interstitial space
    • Reabsorption: fluid moves into capillaries from interstitial space
  • Capillary hydrostatic pressure facilitates outward movement of water from capillary to interstitial space
  • Capillary oncotic pressure (plasma proteins like albumin) attracts water back into capillaries
  • Interstitial hydrostatic pressure facilitates inward movement of water from interstitial space into capillaries
  • Interstitial oncotic pressure attracts water from capillary into interstitial space

Alterations in Water Movement: Edema

  • Edema definition: accumulation of fluid in interstitial spaces
  • Causes:
    • Increased capillary hydrostatic pressure (venous obstruction)
    • Decreased plasma oncotic pressure (loss or reduced production of albumin)
    • Increased capillary permeability (inflammation/immune response)
    • Lymphatic obstruction (lymphedema)
  • Edema distribution: normal distribution between ECF and ICF, with potential 1st space shifting; may progress to 2nd space and 3rd space shifting
  • Examples of 2nd space shifts: ascites, pulmonary effusion
  • Examples of 3rd space shifts: fluid trapped in body compartments with little to no practical gain for perfusion

Edema: Clinical Manifestations and Management

  • Localized vs. generalized edema
  • Dependent edema
  • Pitting edema vs non-pitting edema
  • Third-space swelling; swelling/puffiness; tight clothing/shoes
  • Weight gain is common
  • Treatment approaches:
    • Elevate edematous limbs
    • Compression therapy
    • Avoid prolonged standing
    • Salt restriction
    • Diuretics (as prescribed)

Edema: Practice Question (Illustrative)

  • Question: A patient with hypertension and heart failure has edema in the lower legs and sacral area. The nurse suspects this is due to a(n):
    • Correct choice example: increase in capillary hydrostatic pressure
    • (Other options mentioned: increased plasma oncotic pressure, decreased lymph obstruction pressure, etc.)

Water Balance: Thirst, ADH, and Perception of Hydration

  • Thirst perception is a key driver for water intake
  • Osmolality receptors (osmoreceptors) detect plasma osmolality and signal the posterior pituitary to release ADH
  • ADH actions:
    • Increases water reabsorption in the kidneys
    • Also known as vasopressin
  • Baroreceptors respond to fluid volume deficit and can stimulate ADH release

Water Balance: Antidiuretic Hormone (ADH)

  • ADH is released with: high plasma osmolality or low circulating blood volume
  • Primary effect: increases water reabsorption in renal collecting ducts, reducing urine output

Alterations in Na+, Cl−, and Water Balance

  • Major concepts:
    • Total body water changes are accompanied by proportional electrolyte changes
    • Fluid volume deficit (dehydration/hypovolemia) and fluid volume excess (hypervolemia)

Sodium, Chloride, and Water Balance

  • Sodium (Na⁺):
    • Primary extracellular cation
    • Regulates osmotic forces
    • Regulated by aldosterone and natriuretic peptides
  • Chloride (Cl⁻):
    • Primary extracellular anion
    • Provides electroneutrality
    • Follows sodium

Renin–Angiotensin–Aldosterone System (RAAS)

  • Stimulates sodium reabsorption and potassium/hydrogen ion loss in the kidney (increased Na⁺ reabsorption; K⁺ and H⁺ excretion)
  • Key components:
    • Juxtaglomerular cells release renin
    • Renin converts angiotensinogen to angiotensin I
    • Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II
    • Angiotensin II stimulates aldosterone release from the adrenal cortex
  • Effects on blood pressure and extracellular fluid lengthen:
    • Vasoconstriction (via angiotensin II)
    • Increased blood pressure
    • Increased sodium and water retention
    • Increased extracellular fluid volume
  • Angiotensin II also participates in other pathways affecting kidney and adrenal responses

Aldosterone Release

  • Stimulated by:
    • Low blood pressure (hypotension)
    • Low circulating volume (hypovolemia)
    • Hyponatremia (low Na⁺)
    • Hyperkalemia (high K⁺)

Natriuretic Peptides (NPs)

  • Secreted in response to increased blood volume and pressure
  • Function: oppose the renin–angiotensin system
    • Decreases tubular sodium reabsorption, promoting urinary excretion of sodium
  • Key types: Atrial natriuretic peptide (ANP) and Brain natriuretic peptide (BNP)

Water Balance Question (Illustrative)

  • A scenario: severe diarrhea can affect hormonal responses governing fluid/electrolyte balance
  • Possible responses include changes in aldosterone, renin, ADH, and natriuretic peptides depending on the net fluid/electrolyte status

Hypertonic vs Hypotonic Alterations: Overview

  • Hypertonic alterations (hypernatremia):
    • Serum Na⁺ > 145 ext{ mEq/L}
    • Related to sodium gain or water loss
    • Water moves from ICF to ECF -> intracellular dehydration
    • Manifestations: intracellular dehydration, seizures, muscle twitching, hyperreflexia
  • Dehydration (water deficit):
    • Dehydration (loss of both water and sodium, with overall deficit)
    • Signs: low blood pressure, weak pulse, postural hypotension; elevated hematocrit and serum sodium
    • Headache, dry skin/dry mucous membranes
  • Hyperchloremia: serum Cl⁻ > 106 ext{ mEq/L}
    • Usually secondary to hypernatremia or bicarbonate deficit
    • Managed by treating underlying disorders

Hypotonic Alterations (Decreased Osmolality)

  • Hyponatremia: serum Na⁺ < 135 ext{ mEq/L}
    • Causes plasma hypoosmolality and cellular swelling
    • Clinical categories: hypovolemic, euvolemic, hypervolemic
    • Manifestations: lethargy, headache, confusion, apprehension, seizures, coma
  • Hypochloremia: serum Cl⁻ < 98 ext{ mEq/L}
    • Often results from hyponatremia or elevated bicarbonate

Sodium Imbalances: Brain Focus

  • When thinking about sodium imbalances, think about the BRAIN first due to vulnerability to fluid shifts
  • Watch for red flags: headaches, altered level of consciousness, seizures

Potassium (K⁺)

  • Normal extracellular concentration: 3.5 ext{–} 5.0 ext{ mEq/L}
  • Major intracellular cation
  • Roles: transmission/conduction of nerve impulses, normal cardiac rhythms, skeletal/smooth muscle contraction

Potassium Imbalances

  • Hypokalemia: K⁺ < 3.5 ext{ mEq/L}
    • Causes: reduced intake, increased cellular entry, increased loss
  • Hyperkalemia: K⁺ > 5.0 ext{ mEq/L}
    • Causes: increased intake, shift from ICF to ECF, reduced renal excretion, hypoxia, acidosis
  • Clinical emphasis: think HEART; imbalances produce EKG changes, hypotension, dysrhythmias

Calcium and Phosphate

  • Regulated by three hormones:
    • Parathyroid hormone (PTH): increases plasma Ca²⁺ via renal reabsorption
    • Vitamin D: increases Ca²⁺ absorption from GI tract
    • Calcitonin: decreases plasma Ca²⁺
  • Calcium specifics:
    • Ionized Ca²⁺: 5.5 ext{–}5.6 ext{ mg/dL}
    • Most calcium stored in bone; important for bone structure, teeth, clotting, muscle contraction
  • Hypocalcemia: Ca²⁺ < 9.0 ext{ mg/dL}
    • Causes: inadequate intake/absorption, low PTH or low Vitamin D, blood transfusions
    • Manifestations: increased neuromuscular excitability, muscle spasms, Chvostek sign, Trousseau sign, convulsions, tetany
  • Hypercalcemia: Ca²⁺ > 10.5 ext{ mg/dL}
    • Causes: hyperparathyroidism, excess Vitamin D, immobilization, hypophosphatemia, malignancy, acidosis
    • Manifestations: decreased neuromuscular excitability, weakness, kidney stones, heart block

Phosphate

  • Serum levels: 2.5 ext{–}4.5 ext{ mg/dL} (adult)
  • Location: largely in bone (about 85%)
  • Hypophosphatemia: phosphate < 2.0 ext{ mg/dL}
    • Causes: intestinal malabsorption, renal excretion, Vitamin D deficiency, alcohol use
    • Manifestations: osteomalacia, muscle weakness
  • Hyperphosphatemia: phosphate > 4.5 ext{ mg/dL}
    • Causes: chemotherapy, prolonged phosphate laxatives/enemas, renal failure, secondary to low calcium
    • Manifestations: similar to hypocalcemia with potential soft tissue calcification

Calcium and Phosphate: Reciprocal Relationship

  • Reciprocal balance: when calcium is high or low, muscle symptoms are prominent; think MUSCLE symptoms with calcium imbalance

Magnesium

  • Normal plasma Mg²⁺: 1.5 ext{–}3.0 ext{ mg/dL}
  • Storage: mainly in muscle and bone; interacts with calcium
  • Role: influences neuromuscular excitability
  • Hypomagnesemia:
    • Causes: malabsorption
    • Associated with hypocalcemia and hypokalemia
    • Clinical signs: increased reflexes, tetany, convulsions
  • Hypermagnesemia:
    • Causes: renal failure
    • Signs: skeletal muscle depression, muscle weakness, hypotension, respiratory depression, bradycardia

Magnesium Imbalance: Practical Focus

  • When thinking about magnesium, emphasize neuromuscular signs
  • Watch for: hypomagnesemia (increased reflexes, tetany, tachycardia) and hypermagnesemia (muscle weakness, loss of deep tendon reflexes, hypotension, respiratory depression)

Review Questions (Illustrative Answers)

  • Aldosterone: main function is to promote sodium and water retention and potassium/hydrogen ion excretion; related to decreased blood volume and hyponatremia/hyperkalemia
  • Ascites and third spacing: ascites is third-spacing of fluid often due to decreased oncotic pressure (loss or reduced production of albumin) creating fluid shift into the peritoneal cavity
  • Potassium level 6.1 mEq/L: priority assessment is dysrhythmias, given risk to cardiac conduction

Equations and Key Relationships (Condensed)

  • Osmolar concepts:
    • Osmolarity: ext{Osmolarity} = rac{ ext{total solute particles}}{L}
    • Osmolality: ext{Osmolality} = rac{ ext{total solute particles}}{ ext{kg of water}}
  • Serum sodium and tonicity: hypernatremia/hyponatremia influence water movement across cell membranes and cell size
  • RAAS shorthand (conceptual):
    • Low BP/volume → renin release → angiotensin II → aldosterone → Na⁺/H₂O retention; K⁺ and H⁺ excretion
    • Natriuretic peptides oppose this system to promote Na⁺ excretion

Connections to Practice and Real-World Relevance

  • Understanding fluid shifts helps in recognizing edema, dehydration, ascites, and third-spacing conditions in clinical settings
  • Electrolyte imbalances have wide-ranging effects, especially on cardiac and neuromuscular function
  • Hormonal regulators (ADH, RAAS, natriuretic peptides) are critical in both acute and chronic fluid/electrolyte management
  • Clinical assessment tools include vital signs, neurologic status, edema assessment, urine output/concentration, and targeted labs (Na⁺, K⁺, Ca²⁺, Mg²⁺, Phosphate, Cl⁻, osmolality/osmolarity when indicated)