Ch.7 Fluid and Electrolyte Balance

Division of fluid in our body and cells

• Human body: ~60% water AKA body’s solvent

• Intracellular fluid (ICF): fluid in cells; 40% of bodyweight

• Extracellular fluid (ECF): fluid outside cells, in intravascular spaces; 20% of bodyweight

• Interstitial fluid (ISF): filtrate of blood in between ICF and ECF; mostly contains water and sodium and lacks proteins

Hydrostatic pressure

force of fluid (water) pressure in the bloodstream

• pushes water out from ECF to ICF

Osmotic pressure

Pressure exerted by solutes in solution AKA water magnet because water moves toward particles

• PULLS water from ICF to ECF

When osmotic pressure < hydrostatic pressure = hydrostatic pressure overwhelms

• net force determines fluid’s overall movement direction

Fluid moves from solution with lower osmotic pressure to solution with higher osmotic pressure

Oncotic pressure

Pressure due to albumin in bloodstream AKA colloid pressure

• albumin pulls water into ECF / like osmotic pressure

EX: Hypoalbuminemia = LOW albumin

• means less oncotic pressure pulling water into blood

• BUT hydrostatic pressure is still very STRONG so it keeps pushing water INTO cell

• results in edema

Osmolality

Concentration of solutes/kg in solution

• LOW osmolality = LOW solutes

• HIGH osmolality = HIGH solutes

Osmolarity

Number of osmoles per liter of solution

Tonicity

Amount of solutes in solution compared with bloodstream / tells you whether water moves in or out of cell

• Isotonic: solute concentration inside cell and outside is equal; cell size stays the same

  • blood

  • application: standard isotonic solution = 0.9% NaCl (normal saline) / Ringer’s lactate

• Hypotonic: solute concentration higher inside cell; fluid moves inside cell; cell SWELLS (from ECF to ICF)

  • these solutions have lower osmolarity and lower solute concentration which causes movement of water into cells by osmosis

  • application: 0.45% NaCl as treatment for dehydration / Dextrose 5/0.45% NS which becomes hypotonic once the dextrose is metabolized

• Hypertonic: solute concentration higher outside the cell; fluid moves outside cell; cell SHRINKS (from ICF to ECF)

  • these solutions have higher osmolarity and higher solute concentration so water moves outside the cell

  • application: 3% NaCl (saltwater) - Mannitol infusion used in cerebral edema

Osmoreceptors and ADH

Located in HYPOTHALAMUS and stimulated by increased plasma concentration

• when it notices increase, it tells you to drink water

• initiates thirst mechanism and releases ADH from kidneys (“let’s hold onto our fluids!”)

ADH (vasopressin): released by posterior pituitary gland and tells kidney nephrons to REABSORB water

• ↑ ADH = ↑ water reabsorption = ↑ osmolarity

• ↓ ADH = ↓ water reabsorption = ↓ osmolarity

Fluid homeostasis - Renin Angiotensin Aldosterone System (RAAS)

Body’s system for fixing low BP and low blood volume (SAVE WATER AND TIGHTEN BLOOD VESSELS)

1. Kidneys not receiving enough volume

2. Renin released from kidneys

3. Converts angiotensinogen (from liver) to angiotensin I

4. Angiotensin I converted to angiotensin II in lungs by angiotensin-converting enzymes (ACE)

5. Angiotensin II (vasoconstrictor) squeezes to increase perfusion to kidneys

6. Activates adrenal cortex to release aldosterone

7. Aldosterone increases sodium and water reabsorption and potassium secretion by kidneys

RESULT: ↑ blood pressure ↑ blood volume - ↑ renal perfusion

Fluid Homeostasis - Natriuretic Peptides

Natriuresis: excretes LARGE amounts of sodium and water as a response to excess ECF volume (pulling sink plug)

Peptides that promote natriuresis:

1. Atrial natriuretic peptide (ANP): produced by atrial cells when atria is stretched

2. Brain natriuretic peptide (BNP): produced by heart ventricles and the brain when fluid overload stretches ventricles

3. C-type natriuretic peptide (CNP): produced by endothelial cells of arteries and ventricular cells

Edema

Excess fluid in ICF and ISF caused by…

• elevated hydrostatic pressure = pushing fluid into cells

• Heart failure

  • blood backs up into lungs

  • increased pressure in pulmonary blood vessels

  • fluid gets pushed out of vessels and into lung tissue/alveoli

  • RESULT: pulmonary edema

• vigorous exercise

• vessel obstruction

• alterations in capillary permeability: leaky vessels with larger capillary pores that allow fluid to leave bloodstream into tissue

  • injury and inflammation elicits histamine release which VASODILATES vessels

• decreased osmotic forces in blood

  • hypoalbuminemia from liver failure which may force fluid into third spaces (ascites)

    • no albumin to pull water from ICF to ECF

  • sodium retention: illness, salty foods

    • pulls from from ICF to ECF so you drink more water = increase hydrostatic pressure = edema

Dependent and Pitting Edema

Dependent: fluid accumulates in feet and ankles from increased hydrostatic pressure due to weak valves, lack of muscle contraction or gravity

• prevention: TEDS hose, SCD

Pitting: when pressure is applied to small area and indentation persists after letting go

• severity: +1, +2, +3 seconds

Sequestered fluids

Fluid accumulates in body cavity normally free of fluids AKA third-spacing

• in pericardial sac, peritoneal cavity, pleural space

Fluid entering third space = effusion

• EX: pleural effusion

  • transudate: serous filtrate (clear)

  • exudate: contains blood, lymph, proteins, pathogens, inflammatory cells (murky)

Fluid volume status: OVERLOAD / OVERHYDRATION

Bloodstream has excessive amount of water caused by activation of RAAS due to low perfusion of kidneys

1. heart stops pumping effectively

2. kidneys receive less blood flow

3. RAAS activated

4. sodium + water reabsorbed

5. blood volume ↑

6. hydrostatic pressure ↑

7. fluid gets pushed from ECF to ICF

8. RESULT: edema

KIDNEYS ALWAYS WANT TO WINNNN

• excessive IV administration

• cancer: releases ADH

• cirrhosis: stops producing albumin

• hypertension: excess renin release

• polycystic kidney disease: fluid filled cysts damage kidney function

• SIADH: syndrome of inappropriate ADH - makes TOO MUCH ADH

Fluid volume status: DEHYDRATION

State of diminished water volume in body

• dehydration = hypovolemia

• fluid moves from ICF to ECF causing cells to shrink

• reduced circulating volume / increased blood osmolarity

Decreased circulating volume leads to tachycardia and hypotension

• dark urine, low amount = from ADH, aldosterone

Causes of dehydration

• vomiting and diarrhea

• hot body and sweating: fever, heat stroke, overactive thyroid

• severe burns

• urination

• DI, DKA, Diuretics

  • ↑ glucose = ↑ blood osmolarity

  • water moves toward area with more solutes (ICF to ECF)

  • cells shrink

  • kidneys filter blood and that excess glucose causes excess water to be lost in urine as water is pulled into urine

    • polyuria = excess urine

    • polydipsia = excess thirst

• similar concept with hypernatremia (increased sodium in blood)

  • fluid pulled from ICF into ECF and without replacement, kidneys excrete it

• reduced fluid intake (64 oz per day)

• reduced thirst receptors in older adults

• reduced ADH release (neurogenic DI) / kidneys not responsive to ADH (nephrogenic DI)

Responses to dehydration / hypovolemia

EVERYTHING HAPPENS SIMULTANEOUSLY

• stimulation of osmoreceptors in blood vessels stimulate thirst center in hypothalamus

• stimulation of peripheral baroreceptors lower blood pressure and SNS stimulates vasoconstriction of blood vessels and increased heart rate

• stimulation of kidney to secrete renin = RAAS = raises blood volume and blood pressure

• stimulation of osmoreceptors stimulate posterior pituitary gland of the brain to release ADH, causing water reabsorption at nephron

How to assess fluid status

• daily weight

• 24 hour I&O (1 oz = 30 ml)

• vital signs: HR increase, BP decrease = late signs of dehydration (may cause orthostatic hypotension)

• assess status of mucous membranes, decreased skin turgor, edema

Sodium

• MAJOR ion in ECF

• determinant of ECF osmolarity and volume

• fluid status can affect Na+ ion concentration

Hyponatremia

Normal range: 135-145 mEq/L

HYPOVOLEMIC HYPONATREMIA (loss of fluid and sodium)

• renal causes: adrenal insufficiency, osmotic diuresis, diuretic use, salt losing nephritis (inflammation of nephrons)

• nonrenal causes (primarily GI losses): excessive sweating, diarrhea, vomiting, burns, wounds, cystic fibrosis, fistulas

SXS: thirst, orthostatic hypotension, dry mouth, oliguria, tachycardia

• neurological deficits (seizures) for older adults

TREATMENT: slow replacement of sodium with adequate fluid

HYPERVOLEMIC HYPONATREMIA (loss of sodium WITHOUT loss of fluid)

• SIADH

SXS: headache, lethargy, confusion, muscle cramps/spasms, neuronal cell edema

TREATMENT: correct etiology of excess fluid

Hypernatremia

Sodium level greater than 146 mEq/L

• occurs with excess sodium or decrease in body water

• cells get dehydrated and shrink

• neuronal cells shrink, electrolyte imbalances

• changes in membrane potentials and cell responsiveness

FLUID OVERLOAD - WATER RETENTION

• think kidneys - aldosterone (excess sodium AND excess fluid)

• SX: edema, weight gain, hypertension

NO FLUID OVERLOAD - WATER LOSS WITHOUT SODIUM LOSS

• blood becomes more concentrated

• diabetes insipidus

• SX: thirst, tachycardia, oliguria, flushed, dry mucous membranes

TREATMENT: slow reversal

Potassium

• MAJOR ion in ICF

• normal range: 3.5 - 5.2 mEq/L

• affected by pH

  • acidosis = increased hydrogen ion concentration in blood

  • so H+ moves into cell to buffer blood

  • in exchange, K+ moves out of cell and into blood = hyperkalemia

• involved in muscle contraction, cardiac rhythms, ATP synthesis, neuronal signaling

Hypokalemia

Less than 3.5 mEq/L

Caused by…

• diuretic therapy: pee out too much K+

• mostly from renal system which increase with stress, metabolic alkalosis

  • alkalosis = decreased H+ in blood

  • H+ moves out of cell to make blood more acidic

  • K+ moves into cell

  • hypokalemia in blood

• burns, vomiting, diarrhea, sweat, feces

• large amounts of IV dextrose followed by insulin

• adrenergic agents: epi, norepi, phenylephrine

SXS: anorexia, cardiac dysrhythmias, leg cramps

• digitalis toxicity: K+ and digoxin compete for same binding sites and when there is decreased K+, more digoxin binds to these sites which can increase potential for toxicity

  • green blue halo in vision

• ECG: prolonged PR interval, flattened T wave, prominent U wave

TREATMENT: replace potassium slowly - TOO FAST can cause cardiac arrest (lethal injection)

• IV infusions for potassium burn so you can Y-site infusion to dilute K+

Hyperkalemia

Greater than 5.0 mEq/L

Caused by…

• decreased renal perfusion which can lead to K+ retention

  • in between dialysis days, pts have increased potassium levels

SXS: early symptoms include numbness, muscle cramps, diarrhea

• ECG: wide QRS, tall and peaked T waves, bradycardia

• can lead to cardiac arrest

TREATMENT: sodium polystyrene sulfonate, dialysis, calcium gluconate, sodium bicarb, diuretics

• severe levels: (greater than 7.0) rapid treatment to move K+ from ECF to ICF needed

  • infusion of 50% dextrose and regular insulin drip

    • insulin helps sugar AND potassium enter cells

  • IV sodium bicarb can move potassium from blood into cells

Calcium

• Involved with bones, teeth, blood clotting, neuromuscular signaling

• PTH increase calcium levels

• Calcitonin decrease calcium levels/bring calcium to bones

• calcium and phosphate have inverse relationship

• calcium and magnesium have concomitant relationship

• calcium exists in free and bound forms

  • use albumin levels to interpret calcium levels because calcium is 50% protein bound

  • hypoalbuminemia can cause pseydohypocalcemia

Hypocalcemia

• less than 8.5 mg/dL

• neuromuscular excitability

  • Chvostek’s sign = twitchy cheek

  • Trousseau’s sign = wrist bends inward when taking blood pressure

• paresthesia

• hypotension, cardiac dysrhythmias

• chronic bone pain/fragility

TREATMENT: vitamin D

Hypercalcemia

• greater than 10.5 mg/dL

• causes elevated PTH and cancer from bone destruction

• decreased neuromuscular excitability, weakness, renal calculi (kidney stones), cardiac dysrhythmias

Phosphate

component of bone, RBCs, and ATP

Hypophosphatemia

• less than 2.5 mg/dL

• due to decreased intestinal absorption, increased excretion by kidneys, and intracellular shift

• causes tremors, muscle weakness, hyporeflexia

PHOSPHATE ↓ = CALCIUM ↑

Hyperphosphatemia

• greater than 4.5 mg/dL

• most commonly from kidney failure

PHOSPHATE ↑ = CALCIUM ↓

Magnesium

primarily stored in bone

Hypomagnesemia

• less than 1.5 mEq/L

• caused by sepsis, burns, laxative abuse, diuretics

MAGNESIUM ↓ = CALCIUM ↓

Hypermagnesemia

• greater than 2.0mEq/L

• caused by renal dysfunction

• can present with decreased DTRs, diarrhea

MAGNESIUM ↑ = CALCIUM ↑