SIADH

Too much water inside- concentration of sodium is less (hypokalemia)

Electrolyte increased in renal failure (potassium, phosphate [Decreased calcium])

Calcium= magnesium (hypocalcemia= hypomagnesemia)

Men have greater muscle mass (greater water content)

Women more adipose tissue (more fat)
Older adults decreased water content (45-55% body water left)

What to check if skin turgor is not applicable?

- Tongue
- Check for longitudinal furrows

Body fluids
- 60%
- 2 main compartments (intracellular, extracellular)
- Extra: other compartments: in between cells, plasma (intravascular), transcellular
(very small amounts– pleural, sinovial)

Cations- SPCM
Anion- PHC

Electrolytes inside
Magnesium
Potassium
Phosphate

Diffusion- molecules that move from higher to lower, (ex) place a lump of sugar to a glass of
sugar
Active transport- uses ATP molecules that move against ; electrolyte (phosphorus)
Osmosis- movement of water from lower to higher concentration, (ex) tonicity isotopic (no
movement equal amount– dehydration, no electrolytes involved; for diarrhea also), hypertonic
(more solutes in fluid so the cell will shrink), hypotonic (less molecules because we want the cell
to get the water making the cells swell)
Filtration- movement of water and solutes from high hydrostatic pressure to low hydrostatic
pressure

Hydrostatic pressure (blood pressure)

Oncotic pressure

Solute that gets water from interstitial (albumin)

What triggers thirst?
Thirst - primary regulator of water intake
2 processes:
1. Decreased volume in the ECF
2. Increased osmolality
If you have sensation of thirst → water is absorbed from the GIT

99% of those filtrates are being reabsorbed by the kidneys

RAAS
Maintains intravascular balance and blood volume
Trigger: decrease blood volume thus decreasing blood pressure, then it will trigger the nephrons
to be stimulated and secrete renin
Angiotensinogen - dormant; still asleep
Angiotensin 1 - not significant
Angiotensin 2 - Potent vasoconstrictor
ACE stimulates the adrenal cortex to release ADH

Increase blood volume => ANP released in the atrial muscle cells in the heart primarily affects
the RAS but it opposes/inhibits renin secretions=> diuresis, vasodilation => decreasing the
blood pressure, decreasing the increase blood volume

ADH => increase osmorality => stimulates PPG to release ADH => go to kidneys to reabsorb
more water back to the body => regulates water excretion

Chemical Compounds
SODIUM
a. Extracellular excitation
b. Sodium is abundant in extracellular
c. Primary regulator of volume and osmolality because they are most abundant
d. Low water = increase concentration of sodium
e. Think sodium as the one who excites our cells apart from that they are the ones
who maintains the neuromuscular activities
f. Maintenance of plasma and interstitial osmolality as well as the extracellular
compartment
g. Problems such as hyponatremia => if there are too much water gain inside the
body that could case sodium levels to decrease in concentration => fluid will leak
and goes to the brain cell => increase risk for fluid edema => headache, altered
mental status, muscle cramps, tremors, seizures, coma because of the brain and
nervous system affected by the cellular edema =>
 - MANAGEMENT: fluid excess > fluid restriction, sodium containing foods,
IV therapy, Loop diuretics (because the cause is excess water in which
only the water will go out)
- Hypernatremia
- Manifestation: thirst, increase temp, dry sticky membrane,
restlessness, altered mental status, lethargic, weakness, irritable,
coma and death, decreased LOC
- CAuse: water loss, diabetes insipidus, kidney problems
- MANAGEMENT: intravenous water replacement, IV (Hypotonic),
- DIAGNOSTIC: monitor serum sodium, restrict sodium in the diet
POTASSIUM
- Intracellular excitation
- Regulate cardiac and neuromuscular even skeletal and muscular
- Maintenance of intracellular excitation
- Help maintain acid base balance
- HYPOKALEMIA
- excess potassium loss, conditions, inadequate intake of
potassium, laxative abuse
- MANIFESTATION: weakness, arrhythmia, ECG changes (inverted
ST depression, T wave flattened), nausea vomiting, decrease
bowel sounds, leg cramps (eat banana), muscle weakness
- MANAGEMENT: potassium supplements, increase potassium
foods (banana, avocado, carrots, beans, beef, chicken, salmon,
tuna, lobsters, raisins yuck, oranges, beans, milk, low fat yogurt),
monitor vital signs, monitor the skeletal and muscle strengths,
ECG monitoring
- HYPERKALEMIA
- inadequate renal excretion of k w/ renal failure, other hormonal
conditions
- widened QRS (repolarization occurs more rapidly) cardiac arrest,
vomiting, diarrhea, paresthesia
- Management: elimination/decrease k in the diet, use of diuretics,
dialysis if k levels are very high already
- Medications: calcium gluconate (counter the effects of the cardiac
conduction system), regular insulin, 50 grams of glucose to
promote potassium uptake by the cells

CALCIUM
- Bones and muscle excitation
- Other functions: maintains blood clotting, excitable membranes stabilizer (stabilizing cell
membrane, has sedative effect on neuromuscular transmission)
- Hypocalcemia will have spasms
- Hypercalcemia will have muscle weakness, decreased deep tendon reflexes
Hypocalcemia
- Reduced sedative effect: with hypocalcemia (spams, increased neuromuscular irritability,
chvostek sign– tap on cheek)
- Chvostek sign: tap on cheek, patient’s masseter will twitch
- trousseau sign: inflate bp cuff, leave for 3 mins then there would be a carpopedal spasm
- Also present in hypomagnesemia (+ chvostek and trousseau)
- Serious effects: Tetany, paresthesia, seizures, decreased cardiac output, arrhythmias,
diarrhea
- Oral/ IV calcium chloride, calcium gluconate
- Vitamin D as supplement
- Deep tendon reflexes, muscle spasms, vital signs (esp bp)
- Reason:
- hyperphosphatemia (inverse relationship) due to renal failure– more phosphates
in blood– calcium binds to phosphate
- Undergone thyroidectomy, release of calcium is stimulated by parathyroid
- Renal failure

Hypercalcemia
- Higher calcium levels
- Reasons: increased calcium in bones, excess in parathyroid hormone, increased
intestinal absorption
- Manifestations: decreased muscular excitability, muscle weakness, decreased deep
tendon reflex, altered mental status, decreased consciousness, constipation,
hypertension, polyuria, increased thirst
- Management: eliminate excess calcium, loop diuretics furosemide, sodium phosphate,
IV fluids (isotonic saline)

MAGNESIUM
- A bit similar w/calcium
- Promotes muscle relaxation
- Exerts sedative effect on neuromuscular junction
- Physiological effect affected by potassium and calcium

Hypomagnesemia
- Excited (hyperactive reflexes), tremors, tetany because hypomagnesemia =
hypocalcemia, Chvostek’s sign, trousseau's sign, prolonged pr interval, inverted P wave
- May be because of chronic alcoholism, occurs along with low levels of k and Ca
- Management: monitor for serum electrolytes, monitor GI functioning because it reduces
GI motility, seizure precautions
Hypermagnesemia
- Due to renal failure
- Too much magnesium → muscle relaxation
 - Manifestations: too relaxed, muscle weakness, hypotension, bradycardia, resp
depression, depressed deep tendon reflexes
- Management: treat underlying condition (i.e renal failure), dialysis, calcium gluconate IV -
to reverse neuromuscular and cardiac effect

Phosphate
- Essential for ATP, oxygen delivery and RBC production
- Stimulates muscle contraction, nerve cell transmission, transport

Hypophosphatemia
- There’s paresthesia, muscle weakness, pain & tenderness in the muscles, seizure,
anorexia, dysphagia, decreased bowel sounds → Reduced GI motility, acute resp.
Failure, reduced oxygen delivery
- Lacks ATP, no energy
- Cause: decreased GI absorption of phosphate, refeeding syndrome (this can develop
when a malnourished person is started with enteral/TPN feedings, the glucose in the
formula/solution stimulates insulin release and promotes entry of glucose and phosphate
in your cells thus depleting extracellular phosphate levels), alcoholism, diuretics
- Management: increase phosphate in the diet, treat the underlying cause, encourage the
client to stop with alcohol abuse

Hyperphosphatemia
- Cause: impaired phosphate excretion w/renal failure, shift of phosphate from ICF to ECF
which occurs during chemotherapy problems with regulating of calcium levels
- Manifestations: paresthesia, muscle spasms, tetany, Trousseau’s sign, Chvostek’s sign
- Management: restrict phosphate in the diet, calcium containing antacids, IV therapy

Chloride
- For cellular excitation, maintenance of plasma acid balance, formation of hydrochloric
acid

Hypernatremia
- Manifestations: spasms

Hypernatremia
- Manifestations: weakness

Is dehydration similar to deficit?

- No, because dehydration only refers to water loss but FVD refers to extracellular
and some intracellular fluid loss
FVD
- Diabetes insispud, hemorrhage, inadequate fluid intake
- Leads to hypovolemia
 - Electrolyte involvement (loss) refer it to isotonic fluid volume deficit
- Fluid is drawn into the vascular compartment as your body attempts to
compensate (maintain tissue perfusion)
- Eventually, it depeletes the fluid in the cells because there’s osmosis
- Severe fluid loss leads to cardiovascular collapse
- Weight could be a good indicator as to fluid deficit or gain
- If oyou have weight loss of 2kg = 2L water loss
- Renal failure: Increase 2k weight = 2L fluid gain
- MANAGEMENT: weigh patient daily using same weighing scale at the
same time of the day and use at least same type of clothes, skin turgor,
flat neck veins if the client is recumbent position, IV Therapy
- HYPOTENSION = sign of hypovolemia so monitor BP

Fluid Excess
- Fluid adn water is retained in the body
- Heart failure, renal failure, cirrhosis in the liver (anasarta? = dako tiyan), edema,
hypervolemia and circulatory overload
- MANAGEMENT: administer diuretics (loop[ascending loop of henle | excrete chloride],
thiacide[acts on DCT, excrete sodium chloride, potassium], potassium sparring[excretes
sodium adn water alone]), fluid restrictions, weight monitoring, auscultate lung sounds,
position to fowler position to promote lung expansions to breathe properly.