Homeostasis

- ↑lean body mass = ↑ % of water content

- ↑ adipose tissue = less water content in the body

Body Fluid Compartments

- abt 2/3 of the body water are INTRAcellulaR fluid (ICF), (inside the cells),
- contributes to 47% of the body weight
- interstitial fluid + intravascular fluid (plasma) = EXTRAcellular fluid (ECF)
- abt 1/3 of the body water, ~ 17 % of the body weight
Others: lyphm & transcellular fluid ( CSF, GI fluid, joint spaces, pleural, peritoneal, intraocular & pericardial fluid)

Calculation of fluid gain or loss

 1 L of H2O = 1 kg
 weight change: an good indicator of overall fluid loss or gain
 ex/. A pt receiving diuretic therapy who loses 2 kg in 24 hr has experienced fluid loss ~2L

Distribution of major ions in each compartment

Compartments ICF ECF
Cation K+, small amount of Mg 2+, Na+ Na, small amount of K+, Ca2+,
Mg2+
Anion Phosphate, some protein, small amount og Cl-, small amount of HCO3-,
HCO3- sulfate, phosphate
Processes of Fluid & Electrolyte Movement
Processes Explanation Example of Molecules Is energy required？

Diffusion The movement of molecules from an Gases ( oxygen, nitrogen, NO

area of HIGH LOW concentration CO2), urea
through a permeable membrane
Facilitated The transport of molecule through the Glucose NO
Diffusion cell membrane with the use of protein
carrier from area of HIGH  LOW
concentration
Active Movement of molecule against the Sodium-Potassium pump YES
Transport concentration gradient is used to transport Na out
of the cell & K= the cell
Osmosis Movement of water b/w 2 ONLY H2O NO
compartments separated by a
semipermeable membrane (1 that
allows H2O movement, nut not solute)
- stops when the [] disappears or when
the hysrostatic pressure builds & is
sufficient o oppose any further
movement of H2o
Osmotic Pressure- the amount of
pressure needed to stop the osmotic
flow of water, determined by the
amount of solute in the solution
( mOsm) expressed as osmolarity or
osmolality

Type of Pressure Explanation examples

Hydrostatic Pressure The force within a fluid compartment. In blood vessel, HP is the pressure
The major force that pushes H2O out of the generated by the heart, ↓as the
vascular system at the capillary level blood moves through the arteries
Oncotic pressure/ The osmotic pressure exerted by colloids in Protein in the vascular system
colloidal osmotic solution
pressure Major colloid in the vascular system is
protein, it attracts water, pulling fluid from
the tissue space to the vascular space
Movement of water out of the capillaries are caused by
- Capillary hydrostatic pressure & interstitial oncotic pressure

Movement of fluid  capillary are caused by

- plasma oncotic pressure & interstitial hydrostatic pressure

Shift of Plasma Interstitial Fluid, accumulation of fluid in the interstitium ( edema) occurs if
Pressures
Venous hydrostatic pressure ↑
Plasma oncotic pressure ↓
Interstitial oncotic pressure ↑
How Causes
↑pressure at the venous end of the Fluid overload, HF, liver failure,
capillary inhibits fluid movement obstruction of venous return to
back capillary heart ( tourniquet, restrictive
clothing, venous thrombosis,
venous insufficiency ( manifested
by varicose vein)
Fluid remains in the intersititum if Excessive protein loss ( renal
the plasma oncotic pressure is too disorder), deficient protein
low to draw fluid back capillary synthesis ( liver disease) &
- decrease oncotic pressure is seen deficient protein intake
when the plasma protein content is ( malnutrition)
low
Accumulation of plasma protein in Trauma, burns & inflammation
the insterstitium, ↑ insterstitial
oncotic pressure draws fluid into
the intersittium

Shifts of Interstitial fluid  plasma when there is an ↑ in plasma osmotic or oncotic pressure; happen w/:
- administration of colloids, dextran, mannitol or hypertonic solution, fluid is drawn from the interstitium & H2) is
drawn from cells vis osmosis, which causes equilibration of the osmolality b/w the ICF & the ECF
- ↑ tissue hydrostatic pressure

- ↑ ECF osmolality ( water deficit) : pulls H2O out of the cells until the 2 compartments have similar osmolality
- ↓ECF osmolality: result of gain / retention of excecss water

Fluid spacing: the distribution of body water

First spacing: normal distribution of fluid in ICF & ECF compartments
Second spacing: abnormal accumulation of ISF ( edema)
Third spacing: fluid accumulates in a portion of the body from which it is not easily exchanged w/ the rest of the
ECF
- fluid are trapped & unavailable for functional use. Ex/. Ascites, sequestration of fluid in the abdominal cavity w/
peritonitis, edema asso. w/ burns, trauma, sepsis
Regulation of Water Balance
1) Hypothalamic Regulation
- fluid deficit or an ↑ plasma osmolality is sensed by hypothalamic osmoreceptors, which stimulate thirst &
ADH release
- thirst cause the pt to drink
- hypothalamic ADH is stored in posterior pituitary gland, induce water reabsorption in the renal distal &
collecting tubules
( BOTH ↑ free water in the body & ↓ plasma osmolality. Secretion of ADH is suppressed & urinary excretion is
restored when plasma osmolality is normalized

2) Pituitary Regulation
- hypothalamus control the posterior pituitary gland to release ADH, causes kidneys to regulate water retention.
- factors that stimulate ADH release include ↑ plasma osmolality, stress, nausea, nicotine & morphine
Pathological condition syndrome of inappropriate ADH (SIADH) causes water retention, which causes plasma
osmolality to decrease below the normal value & cause a relative ↑ in urine osmolality w/ decrease in urine
volume
Diabetes insipidus: reduction in the release or action od ADH, causing diluted urine becoz the renal tubules &
collecting ducts do not appropriately reabsorb water
- S:S polyuria, polydipsia, symptoms of dehydration & hypernatremia
3) Adrenal Cortical Regulation (1234)
- ADH affects only H2O reabsorption
- hormones released by the adrenal cortex help regulate bot H2O & electrolytes
- adrenal cortex secretes glucocorticoids ( ex/. Primarilly cortisol) & mineralocorticoids
- glucocorticoids have primarily anti-inflammatory effect & ↑serum glucose lvls, mineralocorticoids ( ex/.
Aldosterone) enhance sodium retention & K+ excretion

- ↓renal perfusion, ↓Na+ in the distal portion of the renal tubule activates RAASm results in aldosterone secretion
- ↑K+ ， ↓ serum Na+ & ACTH stimulates aldosterone secretion, causing the plasma osmolality to ↓ & fluid
volume to be restored

4) Renal regulation
- the kidneys refulate the water balance through adjustment of urine volume
- impaired kidneys cannot maintain fluid & electrolyte balance, results in edema, K+, phosphorus retention,
acidosis & other electrolyte imbalance

5) Cardiac regulation
- Atrial natriuretic factor (ANF)- a hormone release by the cardiac atria in response to increased atrial pressure
( increased volume as in HF), & high serum sodium lvl
- Actions of ANF: vasodilation & ↑urinary excretion of Na & H2O, which ↓ blood volume

6) GI Regulation
7) Insensible Water Loss: an invisible vaporization form the lungs & the skin, helps w/ body temperature
regulation
- the amount of water loss is increased by accelerated body metabolism, as occure w/ body temperature &
exercise
Sensible perspiration/ excessive sweating is caused by fever or high environmental temperatures, may lead to
large amount of water & electrolytes loss

WHAT IS IT?
- Serum Na lvl may become elevated as a result of
WATER LOSS OR SODIUM GAIN
- may cause hyperosmolality, causing shift of water
OUT of the cells cellular hydration
- causing thrist mechanism to be activated
WHAT IS IT?
- result from a loss of Na- containing fluids,
HYPERNATREMIA
HYPONATREMIA water excess in relation to the amount of Na+
(dilutional hyponatremia) or combo of both
- H2O shift out of the ECF cells in response to
hyponatremia asso w/ ECF hypo-osmolality that
results from excess H2O, SHIFT OF h2o  cells
result in cerebral edema

ETIOLOGY
- deficient ADH synthesis in release from posterior pituitary gland ( diabetes SODIUM
insipidus) Etiology
- ↓in responsiveness to ADH (nephrogenic diabetes insipidus) water deficit & - inappropriate use of Na free or hypotonic IV soln
hypernatremia - SIAHD, dilutional hyponatremia results from
- administration of concentrated hyperosmolar tueb feedings & osmotic diuretics abnormal retention of water
( mannitol) - Loss of Na form GI tract, kidneys or skin
- hyperglycemia asso. w/ uncontrolled DM
- excessive sweating & ↑sensible losses from high fever
- excessive soidum intake

Etiology of sodium gain

SIGNS AND SYMPTOMS
- IV adminstration of hypertonic saline/ sodium bicarbonate,
- 1st manifested in CNS: headache,
- use of sodium containing drugs
irritability & difficulty concentrating
- excessive oral intake of Na ( ingestion of seawater)
Severe: confusion, vomiting, seizures,
- primary aldosteronism
coma

Signs & Symptoms Collaborative Care

- changes in plasma osmolality
changes in volume of the cellular water
Neuro: intense thirst, lethargy, agitation,
seizures, coma
- Goal: Tx underlying cause
- Primary fluid deficit: oral fluid or IV infusion w/ isotonic
fluid (0.9 % NS)
- serum Na+ lvl must be reduce gradually to prevent too
rapid shift of H2O back  cells as over rapid correction of
hypernatrmia can cause cerebral edema
Goal of Na excess: dilute the Na [] w/ SALT-FREE IV
fluids ( 5% dextrose in H2O), promote excretion of excess
Na w/ diuretic
- restrict dietary Na intake
COLLABORATIVE CARE
If cause of hyponatremia is caused by H2O EXCESS
- fluid restriction
W/ sever symptoms ( seizure), develops,
- small amount of IV hypertonic saline soln (3% NaCl)
are admin. To restore the serum Na+ lvl
- monitor for response to therapy, serum Na+ lvl
- rapid ↑Na+ lvl can cause osmotic demyelination
syndrome with permanent damage to nerve cells
 ECF vol deficit (hypovolemia) ECF vol excess (hypervolemia)

Causes Abnormal fluid loss Excessive intake of fluid,

(Diarrhea, fistula drainage, abnormal retention of fluids ( HF,
hemorrhage, polyuria), decreased renal failure), interstitial -to-
fluid intake, plasma-to-interstitial plasma shift
fluid shift

Collaborative Care
Goal: correct the underlying causes
- replace both water and electrolytes
- Balanced IV solutions:
- lactated Ringer’s solution, isotonic NaCl is indicated when rapid volume replacement is indicated
- blood is admin when volume loss is caused by blood loss
- diuretics & fluid restriction, Na+ restriction
- abdominal paracentesis/ thoracentesis
Potassium
- critical for cellular and metabolic functions
- for transmission and conduction of nerve impulses,
- maintenance of normal cardiac rhythms, skeletal & smooth muscles contractions
- regulate intracellular osmolality and promote regular growth
- moves  cell during formation of mew tissues & leaves cells during tissue breakdown
- acid-base balance
- dietary sources of K+ from fruits, dried fruit & vegetables
- parenteral sources: IV fluids, stored transfused bloos, & K+ penicillin
- eliminated by kidneys mostly, others lost in stools & sweat
- lvl of K+ may be retained if renal functions are impaired
- there is an inverse relationship between K & Na, factors that cause Na retention ( low blood volume,
↑aldosterone lvl) can cause K+ loss in the urine
- large urine volumes can be asso. w/ excess loss of K in urine

Factors that cause K to move from ECF ICF Factors that cause K+ to move from ICF  ECF

Insulin
Alkalosis
Beta-adrenergic stimulation (catecholamine release
in stress, coronary ischemia, delirium tremens,
administration of B-adrenergic agonist drugs
Acidosis
Trauma to cells ( massive soft tissue damage, tumor
lysis
Digoxin-like- drugs & beta- adrenergic blockings
drugs ( can impair K+ entering into cells), resulting
higher K= lvl in ECF

Rapid cell building (administration of folic acid/

cobalamin ( VitB12) to pt w/ megaloblastic anemia,
results in marked prod of RBCs
P1263

CAUSES
- Abnormal loss of K+ caused by shift of K+ from ECF ICF
- deficiency dietary potassium intake
- abnormal losses via kidneys/ GI tracts via diuresis, elevated aldosterone
lvl （causes retention of Na+ & losses of K+）
- Magnesium deficiency: stimulates renin release & increase aldosterone
lvl, results in K+ secretion
- GI losses of K+ sendary to diarrhea, laxative abuse, vomiting &
ileostomy damage
-Metabolic alkalosis: causes shift of K+  cells in exchange for H+,
thus lowering of K+ lvl in the ECF as in cases of DKA ( RT ↑ urinary K+
loss & shift of K+ cells w/ the admmisntration of insulin & correction
of acidosis
- sudden initiation of cell formation, Ex/. The formation of RBC as in Tx
of anemia w/ cobalamin, folic acid/ erythropoietin
CLINICAL MANIFESTATIONS
- Hypokalemia alters resting membrane potential, ↑negative charges
w/in cells, causing excitability in many tissue
- risk of V-Fib ↑ w/ hypokalemia
- ECG changes to monitor for impaired repolarization: flattening of T
wave & emergence of U wave, ↑amplitude of P wave & may become
peaked
- ↑ digoxin toxicity
- musclce cramps, muscle cell breakdown ( Rhabbdomyolysis)
- myoglobin in in plasma & urine may lead to renal failure
- ↓GI motility ( paralytic ileus), altered airway responsiveness,
impaired regulation of arteriolar BF,
- failure of kidneys to [] urine
HYPOKALEMIA
NANDA
- Risk for injury AEB alteration in
psychomotor functioning (muscle weakness,
WHAT IS IT? hyporeflexia)
-low serum levels of K+ (<3.5
mmol/L)
NURSING IMPLENTATION
- Administration of KCI supplement, ↑dietary intake of KCI
PO/IV
( Note: KCI is NEVER given unless the urine output is at
least 0.5 mL/kg of body wt/ hour, KCl supplements added to
IV solutions should never exceed 60 mmol(mEq/L). The
prefer lvl is 40 mmol.
IV KCl infusion rates should not exceed 10 mEq /hr unless
the pt is in critical care setting w/ cont ECG monitoring &
central line access for administration)
- When given in IV, assess for pain at injection site, & assess
IV sites for at least hourly for phlebitis & infiltration,
infiltration can cause necrosis & sloughing of surrounding
tissue
ECG CHANGES
- ST- segment depression
-flattened T wave, presence of U wave
- ventricular dysrthymias (PVC)
- Bradycardia
- Enhanced digitalis effects)
SAFETY ALERT
- KCl given IV must always be diluted
- NEVER give KCl via IV push or in concentrated amounts
- IV bags containing KCl should be inverted several times to
ensure even distribution in the bag
- Never add KCl to a hanging IV bag, to prevent fiving a bolus
bag

CAUSES
- massive intake of potassium
- impaired renal excretion RT renal failure
- shift of K from ICFECF
- massive cellular destruction (burn, crash injury, tumor lysis)
- rapid transfusion of aged blood
- catabolic state ( severe infection)
- metabolic acidosis ( when the Cl lvl is normal, is asso w/ a shift of
K+ ions from the ICF  ECF as H+ moves in to cells
- Adrenal insufficiency leads to retention of K+ in the serum becoz
of aldosterone deficiency
- K+ sparing diuretics ( spirolactone, triamterene), ACE inhibitors
MANIFESTATIONS
- Hyperkalemia causes membrane depolarization, altering cell excitability
- skeletal muscles become weak or paralyzed
- 1st symptoms: leg cramping
- disturbance in cardiac conduction ( 1st tall, peaked T waves, as K+ ↑,
cardiac depolarization ↓, leading to loss of P waves, a prolonged PR interval,
ST segment depression & widening QRS complex
- irritability, anxiety, abdominal cramping, diarrhea
- weakness of the lower extremities
- Paresthesias, Irregular pulse, cardiac standstill of hyperkalemia is sudden
& severe
HYPERKALEMIA
NANDA
- Risk of Injury AEB alteration in sensation
- potential complication: dysrthythmias
WHAT IS IT?
- high serum levels of
potassium
Nursing Interventions
- eliminate oral & parenteral K intake
-↑ elimination of K, using diuretics, dialysis, use of ion ion-exchange resins
such as sodium polystyrene sulphonate ( Kayexalated), it binds to K+ in
exchange for Na+ & the resin is excreted in feces
- forcing K from ECF ICF, accomplished by administration of IV insulin 9
along with glucose so that the pt does not become hypoglycemia)
- admin IV Na bicarbonate in the correction of acidosis
- rare cases, a beta-adrenergic agonists (epinephrine) is administered
- reversing the membrane effects of the elevated ECF K+ by administering
calcium gluconate IV, calcium ion can immediately reverse the effect of the
depolarization on cell excitability

Nursing implications
ECG changes - monitor ECG changes, dysrhythmias, & effects of therapy
- Tall, peaked T wave, - Adminster IV insulin & glucose, forces K+ cells
- prolonged PR interval - administer IV CALCIUM GLUCONATE immediately if
- ST depression the pt is experiencing dangerous cardiac dysrhythmias
- loss of P waves - hemodialysis
- Widening QRS complex
- V-fib
- Ventricular stanstill