Fluids and Electrolytes: Çøñçëñtråtïøñ åñd Çømpøsïtïøñ Çhåñgës

SODIUM (135 -140 meq/L)

TYPES and CAUSES Treatment
Depletional Hyponatremia
Decreased sodium intake
GI losses
Vomiting
Prolonged nasogastric suctioning Symptomatic Hyponatremia (<120
Diarrhea meq/L): 3% normal saline
Hyponatremia
Renal losses due to diuretics. Asymptomatic Hyponatremia (< 135
(< 135 meq/L)
meq/L but > 120m meq/L): 0.5 – 12 meq/L
Dilutional Hyponatremia per day given slowly
Excessive oral water intake
Iatrogenic intravenous (IV)
Increased secretion of ADH
Drug-induced

Hypervolemic Hypernatremia
Urine Na+ Concentration: >20mEq/L
Urine Osmolarity: > 300 mOsm/L
Iatrogenic administration of sodium-containing
fluids
Hyperaldosteronism (↑ Na+ kidney reabsorption)
Cushing’s Syndrome
Congenital Adrenal hyperplasia
When treating Hypovolemic
Hypernatremia (dehydrated), give
Hypernatremia Normovolemic Hypernatremia
normal saline solution.
(> 145 meq/L) Diabetes Insipidus The decrease in serum Na+ must not
Use of diuretics exceed 1 meq/L per hour
Renal disease
GI or skin water loss

Hypovolemic Hypernatremia
Urine Sodium Concentration: <20mEq/L
Urine Osmolarity: <300 - 400mOsm/L
High serum Na+ levels with decreased extracellular
volume as a result of hypotonic fluid loss
(dehydrated)

SIGNS AND SYMPTOMS (Na+)

Remember the function of sodium: 3 B’s
1. Blood pressure
2. Blood volume
3. pH Balance

HYPONATREMIA – “depressed and deflated”

HYPERNATREMIA – “big and bloated"

dreamiesMD
 Body System HYPONATREMIA HYPERNATREMIA
Headache
Confusion
Restlessness, lethargy, ataxia, irritability, tonic
CNS Hyper or hypoactive DTRs
spasms, delirium, seizures, coma
Seizures, coma
Increased intracranial pressure

Musculoskeletal Weakness, fatigue, muscle cramps/twitching Weakness

Hypertension and bradycardia if significant

CV Hypotension, Tachycardia, syncope
increase in intracranial pressure

GI Anorexia, nausea, vomiting, watery diarrhea -

Dry sticky mucus membranes

Tissue Lacrimation and salivation Red, swollen tongue
Decreased saliva and tears

Renal Oliguria Oliguria

POTASSIUM (3.5 – 5 meq/L)

CAUSES Treatment
Caused by:
Inadequate intake
Excessive renal K+ excretion
Diarrhea
Fistulas
10 meq/L of KCl (if not ECG monitoring)
Vomiting
40 meq/L of KCl (if may ECG monitoring)
Hight NGT output
Hypokalemia Remember that raising/correcting the K+ is
Intracellular shifts
(< 3.5 meq/L) dangerous when there is no ECG
Metabolic Acidosis
monitoring as it could lead to cardiac
Insulin Therapy
arrest.
Drugs
Amphotericin
Aminoglycosides
Cisplatin
Ifosfamide

Increased intake of K+
K+ supplementation (IV or oral)
Blood transfusion
Cell disruption (ex. hemolysis, crush injury, GI
Kayexalate – cation exchange resin that
hemorrhage)
binds K+ in exchange for Na+
Hyperkalemia Glucose and insulin
Increased release of K+ from cells
( > 5 meq/L) HCO3 – correcting acidosis lowers K+
Acidosis
Calcium chloride or calcium gluconate
Rapid rise of EC osmolality (ex. due to glucose)
(give 5 – 10ml of 10% solution)

Impaired excretion of K+
Potassium-sparing diuretics
Renal insufficiency/failure

dreamiesMD
 SIGNS AND SYMPTOMS (K+)
Remember the function of K+:
1. Cardiac
2. Neuromuscular (GI, skeletal and heart)

HYPOKALEMIA – “low and slow”

HYPERKALEMIA – “tight and contracted”

Body System HYPOKALEMIA HYPERKALEMIA

Weakness/Paralysis
Weakness to ascending paralysis
Neuromuscular Fatigue
Respiratory failure
Diminished Tendon Reflex

Hemodynamics
Cardiac arrest ECG changes:
ECG changes: High Peaked T waves
U waves Widened QRS
CV
T waves flattening Flattened P wave
ST segment changes Prolonged PR interval ( AV Block)
Arrthymias with digitalis toxicity Ventricular fibrillation
Hypotension and Bradycardia

Ileus (bowel not moving properly) Diarrhea

GI Constipation (decreased motility) Nausea
Abdominal distention Vomiting

MAGNESIUM (1.7 – 2.2 mg/dL)

CAUSES Treatment
Alterations in intake – starvation, alcoholism,
prolonged alcohol fluid therapy

Renal excretion
Alcohol abuse
Diuretics Magnesium Sulfate 1-2g (though slow IV)
Hypomagnasemia
Amphotericin B during severe deficit (< 1 mgeq/L of Mg)
(< 1.7 mg/dL)
Primary aldosteronism Calcium Gluconate

Pathologic losses (GI losses)

Malabsorption
Diarrhea
Acute pancreatitis

Severe renal insufficiency and parallel changes

in K+ excretion
Hypermagnasemia Excess intake of TPN
Calcium Chloride (5 – 10ml)
(> 2.2 mg/dL) Magnesium-containing antacids and laxatives
Dialysis
Rarely massive trauma
Thermal injury
Severe acidosis

dreamiesMD
 SIGNS AND SYMPTOMS (Mg)
Remember the function of Mg:
1. For law and order of muscles (calm + quiet) – especially neuromuscular and CNS activity
2. Needed to absorbed Vitamin D and Ca2+

HYPOMAGNASEMIA – “no law ang order: buck wild!”

HYPERMAGNASEMIA – calm and quiet organs

Body System HYPOMAGNASEMIA HYPERMAGNASEMIA

Hyperreflexia
Weakness, fatigue
Neuromuscular Muscle tremors
Lethargy
Tetany

ECG changes: Hypotension

Prolonged QT and PR intervals Cardiac arrest
ST segment depression ECG changes:
CV
Flattening or inversion of P waves Increased PR interval
Torsades de pointes (“tornados in the heart”) Widened QRS complex
Arrhythmia (tachycardia) Elevated T waves

Nausea
GI Diarrhea
Vomiting

CALCIUM (9 mg/dL)
CAUSES Treatment
Pancreatitis
Necrotizing fasciitis
Renal failure
Pancreatic and small bowel fistulas TREAT FIRST HYPOMAGNASEMIA
Hypocalcemia
Hypoparathyroidism Caclium Gluconate (IV)
(< 8.5 meq/L)
Toxic shock syndrome Oral Ca2+ tablets
Abnormal magnesium level
Tumor lysis syndrome and rhabdomyolysis
Breast and prostate cancer

BRISK DIURESIS (paihiin lang nang paihiin)

with normal saline
Hypercalcemia
Primary Hyperparathyroidism
(> 10.5 meq/L) Note:
Malignancy (cancer)
Symptoms of hypercalcemia show only
when > 12 md/dL
Critical level: 15 mg/dL

SIGNS AND SYMPTOMS (Mg)

Remember the function of Ca2+: KEEP THE 3B’s STRONG
1. Bones
2. Blood (clotting factors)
3. Beats (heartbeats)

dreamiesMD
HYPOCALCEMIA – “fast and twitch but weak”
HYPERCALCEMIA – “swollen and slow with moans, groans and stones”

Body System HYPOCALCEMIA HYPERCALCEMIA

Muscle cramps
Carpopedal spasm
Stridor Muscle weakness and pain (kasi Ca2+ is
Neuromuscular
Tetany leaving the bones)
Hyperreflexia
Seizures

Hypertension
Decreased cardiac contractility Arrhythmias
Heart failure ECG changes:
ECG changes: Shortened QT interval
CV Prolonged QT interval Prolonged PR, QRS interval
T wave inversion Increased QRS voltage
Heart Block T wave flattening and widening
Ventricular Fibrillation AV block which can lead to complete heart
block and Cardiac Arrest.

(+) Chvostek and Trousseau’s sign Neurologic impairment

CNS
Paresthesias Depression, confusion, stupor, coma

Renal _ Polyuria, Polydipsia

Constipation
Anorexia
GI _ Nausea
Vomiting
Abdominal pain

PHOSPHORUS
CAUSES Treatment
Decrease in phosphorus intake – ex.
malabsorption in GIT or administration of
phosphate binders, malnutrition
Intracellular shift in phosphorus
Hypophosphatemia
Increase in phosphorus excretion Oral of IV supplement of phosphorus
(↑ Ca2+)
Respiratory alkalosis
Insulin therapy
Refeeding syndrome
Hungry bone syndrome

Decreased urinary excretion

Due to impaired renal function
Phosphate Binders (Sucralfate or
Hyperphosphatemia Due to hyper or hypothyroidism
Aluminum containing antacids)
(↓ Ca2+)
Calcium Acetate Tablets
Increased intake of phosphorus
Dialysis
Parenteral hyperalimentation
Phosphorus-containing laxatives

dreamiesMD
Endogenous mobilization of phosphorus
Rhambdomylosis
Tumor lysis syndrome
Hemolysis
Sepsis

dreamiesMD