1/81
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai |
|---|
No analytics yet
Send a link to your students to track their progress
what does fluid balance affect
- Fluid balance affects blood pressure, oxygen delivery, and organ perfusion, and cellular fx
o The body is mostly water, but fluid also contains electrolytes (solutes)
what fx do electrolytes allow?
Nerve signals
Muscle movement
Heart rhythm
fluid balance depends on
- Osmosis
- diffusion
- Filtration
- Pressure
- Kidney regulation
Fluid needs vary by:
- Age → older adults have less total body water than younger adults
- Muscle vs. fat → higher muscle mass=more water and more fat=less water
key fx intracellular fluid
- inside cells (~⅔ of body water)
-Supports cell metabolism, electrical activity, energy
· Imbalance → cells swell or shrink
· Can cause confusion, muscle weakness, dysrhythmias
- Ex: hypo/hypernatremia, severe dehydration → intracellular shifts
key fx extracellular fluid
- Extracellular fluid (ECF) - outside cells (~⅓ of body water)
· Intravascular (plasma)
· Interstitial (between cells)
· Transcellular (CSF, pleural, peritoneal, synovial)
Ex: sepsis, trauma, burns, HF, renal failure causes fluid to move from intravascular into the tissues → seem like they have fluid but are intravascularly depleted → explains why swelling and weight gain can exist along side hypotension and low urine output → why you should never rely on a single assessment finding
dx for ecf
- i and o, daily weights, lung sounds, urine output, hemodynamics, mental status, and lab trends → must all be interpreted together to give the story of where fluid is located and if its supporting circulation
ecf supports
· Blood pressure
· Oxygen delivery
- Nutrient transport
· Medication distribution
what is filtration
Filtration = water movement caused by hydrostatic pressure
Hydrostatic pressure = force fluid exerts against the walls of a space (water-pushing pressure)
If fluid is confined in a space, the pressure increases → The more fluid present = the higher the pressure becomes
Blood pressure is a key example
Water moves: from higher pressure to lower pressure → Continues until pressure equalizes
Occurs across capillary walls
Capillaries are thin and porous
Allow fluid to move easily between the bloodstream and surrounding tissue
High capillary pressure → fluid moves into tissues from vascular space
High tissue pressure → fluid moves back into bloodstream
In critical care: ↑pressure → edema, crackles, ↓ oxygen exchange
Seen in heart failure, sepsis, trauma, fluid overload
what is diffusion
Movement of particles (not water)
Particles (electrolytes, oxygen, glucose) move from high → low concentration until balance is reached
Driven by a concentration gradient
Bigger difference = faster diffusion
Requires a permeable or selective membrane
Capillaries: allow many particles through
Cell membranes: tightly controlled → maintains normal electrical and metabolic function
ex of diffusion
Sodium (Na⁺): higher outside the cell → tightly regulated for nerve & heart function
Glucose: requires insulin to enter cells (facilitated diffusion) → when insulin is absent, the glucose remains in bloodstream
what is osmosis
Osmosis = movement of water only across a selectively permeable membrane in response to a particle concentration
Water moves: Toward higher particle concentration because that side has less water available
Key rule: Water follows solute
Osmotic shifts are a major reason PTs deteriorate quickly
causes of osmosis?
Cell swelling or shrinking depending on the direction of water movement
Changes in blood volume
ex of osmosis
Changes in sodium, glucose, or administered IV fluids can alter osmolarity and trigger rapid movement
what is fluid spacing
Where Fluid Ends up
1st spacing
Normal fluid balance
Fluid evenly distributed between:
ICF
ECF (intravascular + interstitial)
Normal perfusion and circulation
No abnormal fluid accumulation and organ function is normal
2nd spacing
Normal fluid movement into interstitial space
Part of normal capillary exchange → Hydrostatic pressure pushes fluid out of the capillaries, while oncotic pressure pulls it back in
Small amounts of interstitial fluid act as a buffer to help maintain capillary and lymphatic balance
Becomes edema when pressures are disrupted → Hydrostatic pressure increases or oncotic pressure decreases
Fluid is part of normal function and can return to normal circulation and perfusion once the underlying imbalance is corrected
3rd spacing
Fluid shifts out of the bloodstream into areas where it is no longer available to support circulation
Fluid becomes trapped (extensive interstitial edema, peritoneal cavity, pleural space) and unavailable for circulation
Total body fluid may be normal or high
Circulating volume is low
PTs may appear fluid overloaded with obvious edema → BUT intravascularly depleted
s/s of third spacing
HOTN, tachycardia, decreased urine output, s/s of shock → circulation is failing
Edema does not = adequate perfusion
causes of third spacing
Sepsis, severe inflammation, trauma, burns, surgical stress, low plasma protein levels (inflammatory mediators increase capillary permeability → allowing both fluid and protein to leak into tissues → oncotic pressure drops and fluid follows → becomes trapped outside of circulation)
management of third spacing
Restoring intravascular volume
Supporting perfusion
Treating underlying cause of capillary leak while carefully avoiding excessive fluid administration
what is osmolarity
Osmolarity = particle concentration dissolved in body fluids
Normal osmolarity ≈ 300 mOsm/L
When fluids are balanced:
Isotonic
No net water movement
Cells maintain normal size
Key rule: Water follows solute → water moves toward the area with higher particle concentration
key fx isotonic
- No net water movement, fluids are balanced
key fx hypertonic fluid
High particle concentration
Pulls water in
If used inappropriately → dehydrate cells and worsen instability
Ex: When a hypertonic IV fluid is administered, the blood becomes more concentrated → water shifts from cells and interstitial space into the bloodstream to dilute plasma → expands circulating volume → causes swelled cells to shrink
key fx hypotonic fluid
Low particle concentration
Pushes water out
Can lower BP and worsen tissue/cerebral edema
Ex: When a hypotonic IV fluid is administered, the blood becomes more dilute → water shifts out of bloodstream into cells and interstitial tissues → plasma volume decreases and cells swell
what does osmolarity affect
Blood volume
Cell size
Organ function
serum osmolality key fx
- The Big Picture of water balance
- Reflects overall water balance and predicts where water will shift
o Normal: 270-300 mOsm/L → balanced compartments, minimal water movement
o Changes often explain acute mental status changes and perfusion instability
high osmolality
- concentrated blood (fluid deficit) → water moves out of cells into plasma→ cellular dehydration, neurologic risk
low osmolality
o Low osmolality: diluted blood ( excess free water) → water moves into cells → cellular swelling, seizure risk
cations and anions
electrolytes carry these charges → Cations (+) and anions (-)
Balance = electrical stability
body fluids are electrically neutral
electrolytes and fluid compartments
Electrolytes are unevenly distributed between fluids compartments
ECF vs ICF gradients
Gradients allow nerve to fire, muscles to contract, and heart to conduct electrical impulses in a normal function
Required for normal cell function
Small changes = big effects
Confusion, weakness, seizures, dysrhythmias
high risk electrolyte pts
- Older adults
- Kidney/endocrine disease (k increases when kidney fx decreased)
- Diuretics
Key electrolytes to monitor:
• Sodium (Na⁺)
• Potassium (K⁺)
• Calcium (Ca²⁺)
• Magnesium (Mg²⁺)
• Chloride (Cl⁻)
• Phosphorus (PO43-)
key fx na
Major cation in extracellular fluid (ECF)
Primary determinant of intravascular volume
Water follows sodium → Abnormal sodium levels almost always reflect a water imbalance
Normal range: 135 – 145 mEq/L
Key electrolyte for maintaining blood volume, blood pressure, osmolarity and perfusion
low na
(Excess Water → shifts into cells)
Cell swelling →↑Neurologic Risk (Confusion, altered LOC, seizures, cerebral edema)
high na
(water loss → shifts out of cells)
Cell shrinkage → ↑Dehydration
cues for sodium imbalance
- new confusion, restlessness, decreased loc, seizure activity or h/a w/o clear cause, rapid sodium changes over hours not days, sodium abnormalities paired with fluid shifts, diuretics, or iv fluid changes → early warning signs
chloride key fx
Major extracellular anion
Normal: 95-105 mEq/L
Moves with sodium→ reflects fluid status
Supports osmotic balance and acid-base stability (acts as a major counter-ion to bicarbonate)
Helps maintain resting membrane potential of cells
Abnormal levels often signal fluid or acid-base disturbance, not isolated chloride problems
what is elevated chloride associated w?
metabolic acidosis
what is low chloride associated w?
metabolic alkalosis
key fx k
Major intracellular cation → critical for cardiac conduction & neuromuscular function
Normal range: 3.5-5.0 mEq/L
Small changes = big risk → life-threatening dysrhythmias
Kidney dependent electrolyte → always assess renal function and urine output
ecg changes k
- low : flat t waves, u waves
- High: tall, peaked t waves, wide QRS → can progress to heart block or cardiac arrest
clinical cues of potassium imbalance
Rapid potassium shifts over hours (not days), new or unexplained ECG changes, potassium abnormalities in PTs with AKI, CKD, diuretics, ACEI, ARBS, or acidosis should be carefully monitored, rising potassium with decreasing urine output
calcium key fx
Essential for neuromuscular stability, muscle contraction, and blood coagulation
Supports cardiac conduction and nerve transmission
Two types: Bound and Unbound
Regulated by PTH, vitamin D, and calcitonin → control absorption, storage, and release of calcium
low ca
→ tetany, muscle spasms, seizures →
high ca
· High Ca2+ → weakness, dysrhythmias, altered mental status
ionized vs total calcium
Total calcium (includes calcium bound to albumin + free calcium) is affected by albumin → low albumin can falsely lower total Ca2+
Ionized calcium = free active form → most accurate in critically ill patients
clinical cues of calcium imbalances
Neuromuscular irritability, tetany, seizures, cardiac dysrhythmias, low total calcium with low albumin, calcium abnormalities in patients with massive transfusions, sepsis, pancreatitis, or renal failure
mg key fx
Primarily intracellular electrolyte Essential for neuromuscular stability and cardiac rhythm
Essential for neuromuscular stability and cardiac rhythm
Normal range: 1.3-2.1 mg/dL
Works closely with potassium and calcium
cues mg
persistent hypokalemia despite K replacement, unexplained or refractory rhythms, neuromuscular irritability (tremors, increase reflexes), diuretics, alcoholics, malnutrition, sepsis, renal dysfx
low mg
· Low Mg²⁺ → dysrhythmias, muscle twitching, neuromuscular irritability, tremors, hyperrelfexia,
· Required to retain potassium inside the cell
· Low Mg²⁺ can cause refractory hypokalemia
· Often mg must be corrected before K+ or Ca2+ will stabilize
phosphorus key fx
- Energy & Respiratory Strength
· Primary role: ATP production → cellular energy
· Normal: 3.0-4.5 mg/dL
· Regulated by kidneys + bone storage
Increaed risk for resp failure
· Contributes to difficulty weaning from ventilation
· Commonly abnormal in critical illness, renal dysfunction, malnutrition
low phosphorus
Low phosphorus → cells can’t generate energy for normal function → muscle weakness
↓ diaphragmatic strength
↓ respiratory reserve
ICU PTS: Shallow breathing, difficulty weaning from ventilation, increased risk for
clinical cues of phosphorus imbalances
Unexplained muscle weakness or fatigue, difficulty weaning from ventilation despite improving lung status, shallow respirations, phosphorus abnormalities in PTS with malnutrition, refeeding syndrome, sepsis, or prolonged ICU stay, normal potassium and calcium with persistent weakness
what hormones help regulate fluid balance
aldosterone
ADH
ANP/BNP
RAAS
aldosterone key fx
- trigger: low na, low blood volume
- saves na and water, loses k, increases bp
- decreases urine vol
- meaning: increases bp and vol, risk-> fluid retention, hypokalemia
ADH key fx
trigger: high osmolarity, concentrated blood rather than vol
saves water only
urine effect:
High ADH: ↓ Urine, more concentrated
Low ADH: High output, reduced water retention
meaning: dilutes blood, affects na
clinical cues: Low urine output with rising sodium or serum osmolality, sudden changes in mental status, dilutional hyponatremia
ANP/BNP key fx
- trigger: high blood vol, high bp
- dumps na and water
- increases urine vol
- meaning: lowers bp and vol, prevents fluid overload
- clinical cues: Elevated BNP in PTS w/ s/s of overload, persistent edema or crackles despite diuresis, HOTN in PTS aggressively diuresed, worsening renal function during volume removal
RAAS key fx
- trigger: low bp, vol, na, o2 delivery
- saves na and water, vasoconstriction-> triggers aldosterone release
- decreases urine output
- meaning: protects perfusion in shock states
what signals the kidneys to regulate fluids? how do the kidneys adjust?
Hormones (ADH, aldosterone, natriuretic peptides, RAAS) signal the kidneys to decide what to retain or excrete
Kidneys continuously adjust:
Water retention or loss
Sodium and potassium reabsorption
Urine concentration (concentrated vs dilute)
These adjustments maintain blood volume, blood pressure, osmolarity, and perfusion
what is the clearest indicator of the kidney’s response to hormones?
Urine output is the clearest indicator of the kidney’s response
Concentrated urine → conserving volume (↓ perfusion, ADH/aldosterone active)
Dilute urine → excreting excess volume
Urine output must always be interpreted with trends, vitals, labs, and mental status
clinical cues that kidneys are unable to regulate
Decreased urine output despite stable BP, sudden oliguria, anuria, rising creatinine with declining urine output, concentrated urine with signs of hypoperfusion, adequate urine output but worsening mental status or labs, urine output below 400-600 mL/day
Minimum (obligatory) urine output:
~400-600 mL/day to clear waste
BUN
o BUN increases early with low volume or decreased renal blood flow
- ability to clear nitrogen waste, highly sensitive to hydration status and renal blood flow
- High BUN w little or delayed creatinine change: decreased perfusion or volume depletion rather than intrinsic kidney injury
- When rise together: concern shifts to impaired kidney function
creatinine
Creatinine is produced at a relatively constant rate → less affected by fluid shifts
Creatinine = reflects true kidney function
BUN: creatinine ratio
o High ratio = Low circulating volume, renal hypoperfusion
Normal ratio w rising values → intrinsic injury rather than fluid distribution problem
o Both ↑ = Kidney dysfunction
albumin key fx
o Maintains oncotic pressure → keeps fluid in intravascular space
o Low albumin → edema and third spacing
o Patient may look "wet" but be intravascularly depleted
creatinine clearance
Based on 24-hour urine creatinine + serum creatinine
Determines how much blood the kidneys are actually filtering over time
More sensitive than serum creatinine alone for early renal decline
Decreasing CrCl may signal early kidney dysfunction before labs spike
Best interpreted with urine volume, concentration, and trends
what is creatinine clearance equation?
(Urine creatinine x Urine volume) / Serum creatinine
what does creatinine clearance help anticipate?
Medication dosing concerns
Fluid and electrolyte instability
buffers for maintaining ph
- Buffers in the blood immediate response → act immediately to bind or release H ions to limit sudden ph changes → fast but limited capacity, stabilize temporarily
lungs for maintaining ph
· Lungs regulate carbon dioxide (acid) → within minutes, earliest sign of compensation increased ventilation removes co2 to lower acidity, decreased ventilated retains co2 to lower ph
kidneys for maintaining ph
· Kidneys provide long-term control. Manage Acid (H) and Bicarbonate → hours to days, most powerful and sustained correction → accompanied with changes in urine output and electrolytes
-diagnostics: abgs, urine output, lab trends, respiratory patterns
clinical cues of acid-base imbalances
Rapid respiratory changes without an obvious pulmonary cause, acid-base abnormalities paired with electrolyte instability, worsening mental status with subtle ABG changes, rising potassium or falling calcium with acidosis, urine output or kidney markers changing alongside pH shifts
bicarb as neutralizer
Primary base and key buffer in metabolic acid–base balance
Neutralizes acid to keep pH within survivable range
Key principle: ↑ Acid → ↓ Bicarbonate (it is consumed) → metabolic acidosis
Low HCO₃⁻ = metabolic problem
what can low bicarbonate reflect?
Excess acid production
Loss of base
Impaired kidney compensation
what is the clinical significance of bicarbonate?
Falling HCO₃⁻ = ongoing acid production or loss of buffering capacity
Often precedes pH collapse
anion gap key fx
Signals ongoing acid production and limited buffering reserve
Tool used to determine the cause of metabolic acidosis
Compares measured ions to expected balance
what are the ions that are measured?
Sodium is primary measured positive ion
Chloride and bicarbonate are the primary measured negative ions
what is the calculation for anion gap?
Na+ - (Cl- + HCO3-)
normal anion gap
no excess unmeasured acids → suggests bicarbonate loss w chloride replacement
elevated anion gap
Indicates acid accumulation in the blood
Acids consume bicarbonate → bicarbonate level falls and gap widens
Helps answer if metabolic acidosis is d/t acid accumulation or simple bicarbonate loss → elevated anion gap indicates acid accumulation