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)