ELECTROLYTES

 are substances that, when in a solution, separate into ELECTRICALLY CHARGED particles called IONS.
o Cations – are positively charged ions
 Calcium (Ca++), Magnesium (Mg++), Potassium (K+), Sodium (Na+)
o Anions – are negatively charges ions
 Bicarbonate (HCO3_), Chloride (Cl-), Phosphorus (P)
 Electrolytes work with fluids to maintain health and well-being.

ELECTROLYTE IMBALANCES
1. Hyponatremia vs Hypernatremia
2. Hypokalemia vs Hyperkalemia
3. Hypocalcemia vs Hypercalcemia
4. Hypomagnesemia vs Hypermagnesemia
5. Hypochloremia vs Hyperchloremia
6. Hyphosphatemia vs Hyperphosphatemia

SODIUM
 Accounts for 90% of ECF CATIONS
 Most ABUNDANT solute in the ECF
 Normal Serum Na Level – 135 to 145 mEq/L
 inside the cell – 10 mEq/L

FUNCTIONS:
 It helps maintain proper extracellular fluid concentration.
 It helps transmit impulses to nerves and muscles fibers.
 It helps regulate acid-base balance by combining with CHLORIDE and BICARBONATE.

DIETARY SOURCES
 Daily Na requirement – 0.5 to 2.7g
o we consume – 6g/day
o Sodium stays constant – because the more sodium intake, the more Na the kidneys excrete.
o Na – absorbed in the intestines and excreted in kidneys, GI tract, sweat
1. Canned foods
2. Cheese
3. Ketchup
4. Processed meat
5. Salt
6. Salty snack foods
7. Sea foods

REGULATION OF SODIUM AND WATER

Serum Na level DECREASES Serum Na level INCREASES

↓ ↓
Serum osmolality falls Serum osmolality rises
↓ ↓
Thirst diminishes Thirst increases
↓ ↓
ADH release is SUPPRESSED ADH release INCREASES
↓ ↓
Renal water excretion INCREASE Renal water excretion DIMINISHES
↓ ↓
Serum osmolality normalizes Serum osmolality normalizes

HYPONATREMIA VS. HYPERNATREMIA

HYPONATREMIA
• Sodium DEFICIENCY in relation to body water
• SERUM SODIUM LEVEL of < 135 mEq/L
 Serum Na Level decreases
↓
Fluid shifiting occurs
(ECF to ICF)
↓
Hypovolemia
Cerebral edema

CLASSIFICATIONS and CAUSES of HYPONATREMIA

1. DEPLETIONAL HYPONATREMIA
o HYPOVOLEMIC HYPONATREMIA
2. DILUTIONAL HYPONATREMIA
o HYPERVOLEMIC HYPONATREMIA
o EUVOLEMIC / ISOVOLEMIC HYPONATREMIA

DEPLETIONAL HYPONATREMIA
 HYPOVOLEMIC HYPONATREMIA
 A DECREASE in total body WATER with disproportionately GREATER DECREASE in total serum SODIUM
 presence of clinically evident VOLUME DEPLETION

CAUSES:
1. Nonrenal - vomiting, DIARRHEA, excessive sweating, FISTULA
2. Renal - diuretic use, adrenal insufficiency

Adrenal Insufficiency
 hypoactive adrenal glands causing decrease in aldosterone secretion which is responsible for Na and water
retention.

DILUTIONAL HYPONATREMIA – water gain

 HYPERVOLEMIC HYPONATREMIA
 EUVOLEMIC / ISOVOLEMIC HYPONATREMIA

HYPERVOLEMIC HYPONATREMIA
 INCREASE IN TOTAL BODY WATER WITH A RELATIVELY SMALLER INCREASE IN THE TOTAL SERUM SODIUM
 PRESENCE OF CLINICALLY EVIDENT EDEMA
 Cause - HEART FAILURE
o Heart Failure – decreased CO causing a decrease in blood supply to the kidneys which will lead to water
retention

EUVOLEMIC / ISOVOLEMIC HYPONATREMIA

 MILD to MODERATE INCREASE in total body WATER with NORMAL or NEAR NORMAL SODIUM levels
 ABSENCE of clinically evident EDEMA
 Cause – SIADH
o SIADH secretion – syndrome of inappropriate antidiuretic hormone secretion –
 ADH is released even the body doesn’t need it, which results in water retention.
 ADH-induced water retention – volume expansion – secondary natriuresis (ANP) – sodium and
water loss...

SIGNS AND SYMPTOMS (Hyponatremia)

 s/sx are primarily neurologic
1. Headache
2. Nausea
3. Abdominal cramps
4. Muscle twitching
5. Tremors
6. Weakness
7. Changes in LOC – shortened attention span, lethargy, confusion, stupor, coma, seizures
8. S/Sx of hypovolemia (depletional hyponatremia)
o Dry MM, orthostatic hypotension, poor skin turgor, tachycardia
9. S/sx of hypervolemia (dilutional hyponatremia)
o Hypertension, rapid bounding pulse, weight gain
LABORATORY EXAMINATION RESULTS
1. SERUM OSMOLALITY – DEC.
2. SERUM NA LEVEL – DEC.
3. URINE SP. GR. – DEC.

TREATMENT:
1. Restrict fluid intake
2. High Na Foods
3. IVF – NSS if w/ hypovolemia to restore blood volume
4. Intensive Care Unit treatment - < 110 mEq/L
o Hypertonic Solution (D5NSS)
 Monitor carefully for signs of circulatory overload (water shifts from IC to IV) – dyspnea,
crackles, engorged neck veins)
 hypertonic NaCl solution should be administered slowly (furosemide is usually administered at
the same time)

NURSING INTERVENTIONS
1. MONITOR and record V/S
 watch for orthostatic hypotension and tachycardia
2. MONITOR NEUROLOGIC STATUS frequently
 report any deterioration in LOC (lethargy, seizures, coma)
3. Accurately MEASURE and record I &O
 to monitor the effectiveness of therapy
4. WEIGH pt. daily
 to monitor success of fluid restriction
5. ASSESS skin TURGOR for signs of dehydration – at least 8 hours
6. Watch for extreme CHANGES in LAB. RESULTS
7. RESTRICT FLUID as ordered
 dilutional hyponatremia – post a sign in the patient’s room about the restriction
8. INCREASE intake of DIETARY Na
 teach the client about the foods rich in Na
9. ADMINISTER Na SUPPLEMENTS as ordered
10. ADMINISTER IV as ordered
 Isotonic or hypertonic solution
 Watch out for signs of hypervolemia such as dyspnea, engorged neck/hand veins, crackles
11. Provide SAFE environment
 Keep patient safe especially if they have altered thought processes.
 If seizures are likely – pad the bed’s side rails, keep suction equipment handy.

HYPERNATREMIA
 EXCESS of Na RELATIVE to body WATER
 serum Na level of > 145 mEq/L

Serum Na level INCREASES

↓
Fluid SHIFTS occur
(ICF to ECF)
↓
Cellular DEHYDRATION
HYPERVOLEMIA

CAUSES:
 EXCESSIVE sodium intake
o table salts, foods, medications, near drowning, cushing’s syndrome, hyperaldosteronism
 Water deficit
o insensible water losses, extensive burns, severe watery diarrhea, Hyperosmolar hyperglycemic
nonketotic syndrome, diabetes insipidus

SIGNS AND SYMPTOMS

1. Neurologic signs
 Restlessness, agitation, weakness, lethargy, confusion, stupor, seizure, coma.
2. Signs of neuromuscular irritability
 Twitching, hyperreflexia, ataxia, tremors
3. Other signs and symptoms
 Low grade fever, flushed skin, extreme thirst
 Signs of hypervolemia
o Increased BP, bounding pulse, dyspnea
 Signs of hypovolemia
o Dry mucous membrane, oliguria, orthostatic hypotension

Laboratory results
1. SERUM OSMOLALITY – inc.
2. SERUM NA LEVEL – inc.
3. URINE SP. GR. – inc.

TREATMENT
1. OFI – inc.
 Fluids should be given gradually over 48 H to avoid shifting of water into brain cells.
2. IVF – salt-free (D5W), followed by half-NSS (0.45%NaCl)-hypotonic
 If the client can’t drink enough fluid, he’ll need IVF (Dextrose 5% in water followed by Half- NSS to
prevent hyponatremia (which can lead to cerebral edema)
3. Diet – restrict Na
4. Diuretics - inc. Na loss

NURSING INTERVENTIONS
1. Monitor and record V/S
 hypervolemia – elevated BP, bounding pulse, dyspnea
 hypovolemia – dry MM, oliguria, orthostatic hypotension
2. INSERT IVF as needed
 Hypotonic – WOF signs of cerebral edema (n/v, seizure, coma).
 Report any deterioration in LOC
3. MEASURE and record I & O and weigh patient daily to check fluid status
4. Assess SKIN and MM for signs of dehydration
5. Assist ORAL HYGIENE
 lubricate lips with water-based lubricant and provide mouth wash or gargle.
 Good mouth care helps keep mucus membranes moist and decreases mouth odor.

Potassium (K)
 major cation in the ICF
 98% - is in ICF
 2% - in ECF
 Potassium imbalance affects nerve impulse transmission
Normal Serum K level is 3.5-5mEq/L

Roles of K in the body

 maintains cells’ electrical neutrality and osmolality
 Aids in neuromuscular transmission of nerve impulses
 Assists in skeletal and cardiac muscle contraction and electrical conductivity
 Affects acid- base balance

Dietary sources of K
 K must be ingested daily because the body can’t conserve it.
1. Chocolates
2. Dried – fruits, nuts and seeds
3. Fruits – oranges, bananas
4. Meats
5. Vegetables – potatoes, mushrooms, tomatoes, carrots

Balancing K
 80% of K intake is excreted in the urine, the rest is excreted in feces and sweat
 Anabolism (constructive process) – K moves from ECF to ICF
 Sodium-Potassium pump – moves Na from the cell into the ECF and pumps K into the cell
 Na and K – have a reciprocal relationship
 pH – Hydrogen ions and K ions freely exchange across plasma cells.
o For example, in acidosis – increase in H ions
o The excess hydrogen ions move into cells and push K into the ECF causing hyperkalemia (and vice versa)
HYPOKALEMIA VS HYPERKALEMIA
HYPOKALEMIA HYPERKALEMIA

Serum K < 3.5mEq/L >5mEq/L

HYPOKALEMIA HYPERKALEMIA

CAUSES: > Inadequate K intake > Too much intake

(not eating enough K-rich foods, receiving
K-deficient fluids)
> Too much output
(GI suctioning, lavage, prolonged vomiting,
diarrhea, diuresis)
drugs > diuretics, corticosteroids, insulin
(diuretics – inc urination;
corticosteroids – Na retention, K excretion;
Insulin – moves K from ECF to ICF)
Diseases > alkalosis, malabsorption syndrome
(alkalosis shifts K from ECF to ICF;
Malabsorption decreases K absorption)
(increased dietary intake of K esp with
decreased urine output; too much K
supplements)
> Little output
(renal failure)
> beta-blockers, k-sparing diuretics,
chemotherapy
(beta-blockers – which inhibits K shifting into
cells; k-sparing diuretics; chemotherapy – lyses
malignant cells causing K to shift from ICF to
ECF)
> Severe infection, trauma/crush injury.,
acidosis, insulin deficiency
(Severe infection and trauma shifts K from ICF to
ECF;
insulin deficiency – inc K in ECF)
> Blood transfusion
(the serum K level of donated blood increases
the longer the blood is stored)

s/sx Hypokalemia Hyperkalemia

Neuromuscular > Skeletal muscle weakness > Skeletal muscle weakness

GIT > constipation, paralytic ileus > nausea, diarrhea, abdominal

cramping

Changes in ECG (can cause > Flattened T wave, depressed ST > tall, tented T wave
arrhytmias) segment, characteristic U wave

DAIGNOSTIC TESTS HYPOKALEMIA HYPERKALEMIA

Serum K level < 3.5 mEq/L > 5mEq/L

ABG Result Elevated pH and HCO3 Decreased pH

Elevated serum glucose level

TREATMENT (Hypokalemia)
1. Diet – high K diet
2. Oral K supplements
 KCl (Kalium Durule)
 Administer with food / 4 oz of fluid to avoid gastric irritation
3. IV k replacement therapy
 Never give K by IV push or bulos (can cause cardiac arrhythmias and cardiac arrest)
 Incorporated in the IVF
  Monitor urine output - >30ml/hour to avoid hyperkalemia
 Watch the IV infusion site for infiltration – can irritate veins and cause discomfort

TREATMENT (hyperkalemia)
1. diet – restrict K
2. Diuretics – loop diuretics (furosemide – lasix) – employ BP precautions
3. D/C medications associated with high K levels
4. Hemodialysis
5. Drugs – sodium polystyrene sulfonate (kayexalate)
 Kayexalate (oral, NGT, enema)
 A cation exchange resin
 As the medication sits in the intestines, Na moves across the bowel into the blood, and K moves out of the blood
into the intestines.
 Loose stools remove K from the body
6. Emergency cases (>6mEq/L) – can lead to serious cardiac arrhythmias, cardiac arrest
 Closely monitor cardiac status
 Administer 10%Calcium Gluconate
o To counteract the myocardial depressant effects of hyperkalemia
o slow IV infusion
 Acidosis – administer sodium bicarbonate
o To neutralize blood acidity
o Check for the patency of the IV site
o Flush IV line with NSS before and after administration (can inactive many drugs or cause them to
precipitate)
 Administer 10 units regular insulin IV
o WOF hypoglycemia – muscle weakness, syncope, hunger, diaphoresis

NURSING INTERVENTIONS (Hypokalemia )

1. Monitor VS
 esp pulse and BP – weak, irregular; orthostatic hypotension
 HR – WOF tachyarrhytmias
 RR – WOF shallow and rapid respiration
o notify MD – be ready with emergency kit (ambu bag, endotracheal tube, oxygen, mech vent)
2. Monitor serum K levels
3. Monitor I and O
4. Check for signs of alkalosis – irritability and paresthesia
5. Insert and maintain an IV access as ordered
 WOF infiltration at IV site because k can irritate surrounding tissues
6. Provide safe env’t
7. Check for signs of constipation because of hypoactive bowels
8. Health teachings:
a. Importance of taking K supplements as prescribed
b. If client is on digoxin therapy, teach patient to recognize and report s/sx of digoxin toxicity (pulse
irregularities, anorexia, N/V)
c. Make sure the client can identify the signs and symptoms of hypokalemia

NURSING INTERVENTIONS (Hyperkalemia)

1. Assess VS
 anticipate cardiac monitoring if the patient’s serum K level exceeds 6mEq/L
2. Monitor I and O
 report output of less than 30ml/hour (inability to excrete K may lead to dangerously high K levels)
3. Prepare patient for dialysis – esp for acute hyperkelamia
 check the vascular access site every 2 hours for patency and signs of clotting, feel for a bruit
 Check the site for bleeding after dialysis
 NO BP taking in the AV fistula site, nor drawing blood or inserting IV catheter
4. Implement safety measures
5. Health Teachings
a. Select foods that don’t stimulate peristalsis – avoid caffeinated drinks and high roughage diet
b. Explain S/Sx of hyperkalemia (muscle weakness, diarrhea, nausea, hypotension, etc)
MAGNESIUM
 After K, magnesium is the 2nd most abundant cation in the ICF
 Bones – contain 60% of the body’s magnesium
 ECF – 1%
 ICF – holds the rest

IMPT. FUNCTIONS OF MAGNESIUM IN THE BODY

 Promotes enzyme reactions within the cell during carbohydrates metabolism
 Helps the body produce and use ATP – for energy production
 Takes part in protein synthesis
 Influences vasodilation, helping the Cardiovascular system function normally
 Helps sodium and potassium ion cross the cell membranes
 Magnesium also regulates muscle contraction
o Mg acts on the neuromyonal junctions (sites where nerves and muscle fibers meet)- Mg affects the
irritability and contractility of cardiac and skeletal muscle.
 Magnesium influences calcium level
o Mg influences Ca level through its effect on parathyroid hormone (PTH).
o PTH- when serum Ca level decreases parathyroid glands release PTH (pulls Ca out of the bone into the
ECF)
o Low Mg causes low PTH and in turn causing low serum Ca level
 Normal Serum Magnesium Level
o 1.6 to 2.6 mEq/L
 Inside the cells – about 40mEq

HOW THE BODY REGULATES MAGNESIUM

 The GI and urinary systems regulate magnesium through absorption, excretion and retention.
 Through dietary intake and output in the urine and feces
 A well-balanced diet should provide roughly 25 mEq (300 to 350 mg) of magnesium daily
 40% of this is absorbed in the small intestines

DIETARY SOURCES OF MAGNESIUM

1. Chocolate
2. Dry beans and peas
3. Green, leafy vegetables
4. Meats
5. Nuts
6. Seafoods
7. Whole grains

HOW THE BODY BALANCES MAGNESIUM

 The body tries to adjust to any changes in magnesium level
1. GIT - If the serum Mg level drops – GIT absorb Mg And V.V.
2. Kidneys – balance Mg by altering reabsorption at the proximal tubule and loop of henle
 If serum Mg level rises – the kidneys excrete excess in the urine

HYPOMAGNESEMIA
 Occurs when the body’s serum magnesium level falls below 1.5mEq/L

CAUSES:
1. Poor dietary intake of Mg
 Chronic alcoholics
 NPO Patients
2. Absorption problems
 Poor GI absorption
 malabsorption syndrome, bowel resection
3. GI Problems
 Prolonged diarrhea, laxative abuse, NGT
 Fluid in the GIT (esp lower part) contain Mg...
4. Urinary Problems
 Prolonged administration of diuretics
 Loop diuretics (furosemide – lasix) – acts on ascending loop of henle to prevent water and na reabsorption
 DM – increased urination
SIGNS AND SYMPTOMS:
1. CNS S/SX - A low serum Mg level irritates the CNS leading to:
Altered LOC hallucinations
Ataxia insomnia
Confusion psychosis
Delusions seizures
Depression vertigo
emotional lability
2. NEUROMUSCULAR S/SX
 low serum Mg – body compensates by moving Mg out of cells (cells become Mg starved, skeletal muscles grow
weak and nerve and muscles become hyperirritable)
 Skeletal muscle weakness
 3Ts
Tremors
Twitching-slight, sudden movement that is not controlled or deliberate
Tetany – involuntary contraction of muscles
 Hyperactive DTR
 Foot or leg cramps
 Paresthesia – a sensation of pricking, tingling or creeping on the skin that has no objective cause.
 Breathing difficulties – laryngeal stridor (high-pitched breath sound)
o Narrowed airway (laryngeal spasm) – from muscle weakness and hyperirritable nerves and muscle
3. signs of Hypocalcemia
o Decrease in Mg causes decreased PTH – dec Ca
 CHVOSTEK’S SIGN- facial twitching when facial nerve is tapped
o tap the facial nerve adjacent to the ear – brief contraction of the upper lip, nose, or side of the face
 TROUSSEAU’S SIGN – carpal spasm when upper arm is compressed
o apply BP cuff to the patient’s upper arm (inflate up to 20mm Hg) – after 1 to 4 mins – patient will
manifest adducted thumb, flexed wrist and extended fingers
4. CV S/Sx
o Tachycardia , arrhythmias
 Decrease in Mg causes myocardial irritability leading to arrhythmias (irregular heart beat), tachycardia
o Hypertension
o ECG changes
 Prolonged PR interval
 Widened QRS complex
 Prolonged QT interval
 Depressed ST segment
 Broad, flattened T wave
 Prominent U wave
 TORSADES DE POINTES
o As the Mg level drops, myocardial sensitivity increases, leading to lethal arrhythmias called torsades
de pointes

o
5. GI S/SX
 Anorexia
 Dysphagia-difficulty in swallowing
 Nausea/ vomiting

6. Digoxin Toxicity - Low Mg level may increase the body’s retention of digoxin- WOF digoxin toxicity if patent is
receiving digoxin
 anorexia
 N/V
 Yellow-tinged vision
 Arrhythmias
DIAGNOSTIC EXAMS:
1. Electrolyte Abnormalities
 hypocalcemia (because of the effects of Mg to PTH),
 decreased Mg levels
 2. Characteristics ECG changes
 Prolonged PR interval
 Widened QRS complex
 Prolonged QT interval
 Depressed ST segment
 Broad, flattened T wave

TREATMENT:
1. Increase dietary intake of magnesium
2. Magnesium Supplements
 Magnesium Chloride (MgCl) – taken with meals (to avoid s/e such as stomach upset and diarrhea)
3. Magnesium Sulfate – IV or IM
 For severe hypomagnesemia (below 1mEq/L)
 Assess renal function before administration
 Urine output should be monitored q 4h – MgSO4 is not given if <10ml for 4 hours
 Check for hypermagnesemia – hypotension, respiratory distress
 Keep calcium gluconate (antidote) – cardiac or respiratory arrest (HAVE RESUSCITATION EQUIPMENT NEARBY)

NURSING INTERVENTIONS:
1. Assess for mental status and report changes
 low serum Mg level irritates the CNS causing altered LOC, seizures
2. Evaluate the patient’s neuromuscular status regularly
 hyperactive DTR, tremors, tetany, Signs of hypocalcemia
3. Check for dysphagia before food is given
 Hypomagnesemia may impair ability to swallow
4. Monitor and record VS
5. Monitor respiratory status
 hypomagnesemia can cause laryngeal stridor and can compromise airway
6. If patient is receiving digoxin, monitor for signs of digoxin toxicity
 Magnesium deficiency enhances the pharmacological action of digoxin – toxicity (nausea, vomiting,
bradycardia)
7. Institute seizure precautions.
 Provide calm, quiet environment; room-dimly lit; avoid unnecessary handling the patient
8. Keep emergency equipment nearby for airway protection
 Endotracheal tube, laryngoscope, O2

HYPERMAGNESEMIA
 occurs when the body’s serum Mg level rises above 2.5mEq/L.

CAUSES:
1. Excessive Mg intake
 common in patients with renal failure who use Mg containing antacids or laxatives.
 Antacids – Maalox laxative – Milk of Magnesia Magnesium Supplement – Magnesium Sulfate
 Continuous infusion of Mg Sulfate to treat Pregnancy-induced Hypertension
2. Renal Dysfunction– advancing age, renal failure

Signs and Symptoms:

 High serum Mg level depresses the neuromuscular system
1. Decreased muscle and nerve activity – hypoactive DTR
2. Generalized weakness – starts with weak hand grasp (progresses to flaccid paralysis)
3. Occassional N/V
4. dec. LOC – drowsy – coma (Excess Mg depresses the CNS)
5. Respiration – slow, shallow, depressed (Excess Mg weakens respiratory muscles - respiratory arrest – mech vent)
6. Weak pulse, bradycardia, arrhythmias - dec. CO and cardiac Arrest
7. Hypotension, pt feel flushed and warm all over (caused by vasodilation)
HYPERMAGNESEMIA
 High Mg level – depresses the neuromuscular system
Magnesium level Signs and Symptoms presented
3mEq/L  Feeling of warmth
 flushed appearance
 Mild hypotension
 NV
4mEq/L  diminished DTR
 Muscle weakness

5mEq/L  Somnolence-state of being drowsy; sleepiness

 ECG changes
 Bradycardia
 Worsening hypotension

7mEq/L  Loss of DTR

8mEq/L  Respiratory compromise

12mEq/L  Heart block
 Coma

15mEq/L  Respiratory arrest

20mEq/L  Cardiac arrest

Diagnostic Tests:
1. Serum Mg level – inc
2. ECG – prolonged PR interval, widened QRS complex, tall T wave

Treatment:
1. Increase fluid intake – oral or IV
Inc fluid intake if pt has normal renal function to inc urine output, getting rid of excess Mg
2. Loop diuretic
3. Ca Gluconate – a Mg antagonist
 D5W (never dilute with solutions containing bicarbonate – causes precipitation
 avoid giving Ca diluted in NSS – NaCl increases renal calcium loss
 never give it rapidly – syncope(LOC resulting from insufficient blood flow to the brain) , hypotension,
arryhythmias
 WOF symptoms of hypercalcemia – anorexia, NV, lethargy, confusion
 observe IV site for signs of infiltration – can cause tissue sloughing and necrosis
4. Hemodialysis – use Mg-free dialysate

Nursing Interventions:
1. Monitor VS
 Watch out for hypotension, respiratory and cardiac arrest
2. Assess Neuromuscular system
 Watch out for diminished DTR, weakness and decreased LOC
3. Restrict dietary Mg intake & avoid giving meds with Mg
 Post “No magnesium product” at the door of the patient’s room or at the bed of the patient
4. Provide adequate fluids – oral / IV
 Increasing fluid intake will increase urine output and will rid excess Mg