NOTE HYPER HYPO

• Major extracellular cation

Sodium
Thirst is the body’s main defense
Primarily neurologic symptoms

• Attracts fluid and helps preserve fluid volume

may result from diabetes insipidus ( inadequate ADH )
Headache, Nausea/Vomiting, altered mental status, stupor, seizures,
• Combines with chloride and bicarbonate to help Mainly neurological symptoms ( Signs of associated hypo or hypervolemia)
coma

135 - 145 mEq/L regulate acid-base balance

Think S-A-L-T
• Hypovolemia

Skin flushed / seizures

poor skin turgor, tachycardia, decreased BP, orthostatic hypotension

Agitation

Low grade fever

• Hypervolemia

Thirst edema, hypertension, weight gain, bounding tachycardia

- Correct underlying problem (if known)

MILD CASE
- hyper/isovolemic: Restrict fluid intake
- Gradual hypotonic fluid replacement (to avoid brain edema) each 4 H
- Hypovolemic: increased Nat intake (IV or oral)

- Monitor for s/s of cerebral edema

SEVERE CASE
- Infuse hypertonic NaCI solution (3%NaCI)
- Monitor serum Na+ level every few hours
slowly (both case slowly hype +hyper)
fast correlation results in Edema or pontain demylination Especialy with
- Seizure precautions hyper.
- Furosemide to remove excess fluid Diuritics
- Monitor in ICU
- Treat the underlying cause

Potassium
Major intracellular cation
Caused by
caused by

Hypo or hyperK+ can lead to serious neuromuscular - Renal failure (90% urine )

and cardiac problems - Increased intake (food rich in K+ or salt substitute + renal impairment)
- GI losses (vomiting, diarrhea, ileostomy, …)

3.5 – 5.5 mEq/L - Blood transfusion ( k inside RBC hemolysis when transfusion and blood have - non-K+ sparing diuretics (thiazide, furosemide)

Most ingested K+ is excreted by the kidneys (~90%) expiration date

- insufficient intake (IV fluids without K+…)

urine - Drugs (K+ sparing diuretics, ACEI, …)

patient with renal impairment at higher risk of

- Extensive trauma, hemolysis, rhabdomyolysis, reperfusion injury…
hyperkalaemia, cardiac arrest and death
(intracellular k go out )

Increased K+ = Aldosterone secretion = Na+ • Muscle weakness (especially legs)

Skeletal muscle:
reabsorption and K+ excretion
weakness

• Smooth muscles: ( contraction ) Nausea, abdominal cramps, diarrhea

NEVER GIVE IV PUSH Smooth muscles: ( weakness )

• ECG changes (tented T wave with narrow base, prolonged P-R, loss of P - constipation, ileus

Mix well when adding to an IV solution bag

wave, shortened QT interval, ST-segment depression, heart block, cardiac
Rates usually 10-20 mEq/hr, not to exceed 40 mEq/h
arrest)
Cardiac muscles:
“40 in 400 over 4 h”
• Hypotension
- ECG changes (flattening and inversion of T wave, Q-T prolongation,
“40 in 500 over 2 h”

widearscouplex visible U wave, ST depression, Torsades de points, ventricular

tachycardia)

Hypertension don't give NaCL give KCL to decrease

pressure but when there is renal impairment ( increasing
peakeatwave - Digitalis toxicity

- Orthostatic hypotension

K )

more potassium you eat, the more sodium you

r
lose through urine.

Mild • Increase dietary K+

Loop diuretics (Lasix)

• Oral KCl supplements

Dietary restriction
• IV K+ replacement

to shift K+ from extra to intracellular space

• Change to K+-sparing diuretic (spironolactone)

• Monitor ECG changes

Moderate • Treat underlying causes

chelating agents :

Calcium polystyrene sulfonate (e.g. Sorbisterit, Ca-Resonium)

Sodium polystyrene sulfonate (e.g.Kayexalate, Anti-Kalium-NA)

Emergency
10% calcium gluconate
IV over 2-3 min. to protect the heart

Sodium bicarbonate (brady cardia, Heat block) transit protection

Alkaline blood to shift K+ from extra to intracellular space

IV Glucose + insulin gla-K to Intracel

to shift K+ to intracelluar shifting

Salbutamol nebulizer

Chelating agents

Hemodialysis LAST CHOICE

monitoring the ICU

• Helps produce ATP

Not common
Causes:

Magnesium Causes :
- poor dietary intake

1.5 – 2.5 mEq/L • Role in protein synthesis & carbohydrate metabolism

- Renal dysfunction (most common cause)
- poor GI absorption

- Iatrogenic ( food )
- Chronic alcoholism

• Helps cardiovascular system function (vasodilation)

- Addison’s disease, Adrenocortical insufficiency, Untreated DKA
- excessive GI/urinary losses (diuretics, stoma, diarrhea…)

- Prolonged IV fluids without Mg++

• Regulates muscle contractions

Decreased neuromuscular activity

CNS : LOC, confusion, hallucination, seizure

• Respiratory failure
CVS : tachycardia, HTN, ECG changes

• Generalized weakness
Neuromuscular: muscle weakness, leg cramps, tetany, Chvostek's sign ,
trousseau's sign

• nausea/vomiting names.name GI: dysphasia, anorexia, N+V

• IV fluids (if renal function is normal)
Mild
• Loop diuretics (get rid of Mg++)
Dietary supplements

• Calcium gluconate

• Mechanical ventilation for respiratory depression

Severe
• Hemodialysis
IV magnesium sulfate infusion pump

Monitor ECG and symptoms

99% in bones, 1% in serum and soft tissue (measured by

Main causes:
Causes:

calcium serum Ca++)

Cancer (Mets, tumors producing PTH like peptides) commonest cause in hospitalized
pt

- Inadequate intake

- Malabsorption

4.2 - 5.2 mEq/L

~50% ionized (1.1 – 1.3 mmol/L) Active form
- Hypoalbuminemia (low total but normal ionized)

~50% non ionized is bind to proteins

Hyperparathyroidism commonest cause in general
- Acute pancreatitis
2.1 - 2.6 mmol/L
- thyroid or parathyroid surgery

‫كتف فورم عالي او‬.‫ ممكن يكون عندي التوتل للكالسيوم نورمال بس ا‬Prolonged immobilization
- loop diuretics - Blood transfusion (citrate)

8.5-10.5 mg/dl ‫ واطي مشان هيك بصير عندي‬hyper or hypo - hypomagnesemia ( mg have roll in releasing PTH )
Addissonian crisis
Role in contraction of all types of muscles

Participates in blood clotting

Levels regulated and affected by: PTH, vit-D, calcitonin,

serum Albumin

Fatigue, confusion, lethargy, coma

Anxiety, confusion, irritability

Muscle weakness, hyporeflexia

Neuromuscular

hyperreflexia, muscle twitching, paresthesias (peri-oral, fingers, toes) , tetany,

Hypertension • Bradycardia cardiac arrest
convultions, Chvostek’s sign, Trousseau sign

Anorexia, nausea/vomiting ,ileus, constipation Diarrhea

Polyuria*, renal calculi, renal failure Diminished response to digoxin

Peptic ulcer ECG changes

treat underlying cause (CA, PTH, …)

Calcium gluconate IV
Adequate hydration with IV fluids

Oral calcium and vitamin D

Loop diuretics (to kick out Ca++)

Monitor ECG and for convulsions if necessary

Corticosteroids

The primary anion in the intracellular fluid

Causes:
Can cause acute respiratory failure and need for MV

Phosphorus Crucial to cell membrane integrity, muscle function,

- Impaired kidney function

- Cell damage, hemolysis, extensive trauma

Causes:

1 - 1.5 mmol/L neurologic

- Hypoparathyroidism
respiratory alkalosis (hyperventilation)
- Respiratory acidosis Excessive insulin release, and refeeding syndrome

function and metabolism of carbs, fats and protein •

- Increased dietary intake
Malabsorption

Diuretics

Functions in ATP formation, phagocytosis, platelet function Hyperparathyroidism

and formation of bones and teeth

Extensive burns

Arrythmias
Musculoskeletal

muscle weakness respiratory muscle failure

Hyperreflexia

Cardiac

Muscle weakness
hypotension decreased cardiac output

Oliguria
CNS

confusion, anxiety, seizures, coma

Low-phosphorus diet
MILD/MODERATE

Dietary modifications Oral supplements

Decrease absorption with antacids that bind phosphorus

SEVERE

Treat underlying cause of respiratory acidosis or DKA

IV replacement using potassium phosphate or sodium phosphate

IV saline for severe hyperphosphatemia in patientswith good kidney function

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