ELECTROLYTES

• Chemical compounds in solution that

have the ability to conduct an electrical
current
• Break into charged particles called
“ions”
• Positively charged: CATIONS
• Negatively charged: ANIONS
– ECF: major CATION- Na; major ANION- Cl
– ICF: major CATION- K; major ANION-
HPO4 & SO4
Functions

• Promote neuromuscular irritability

• Maintain body fluid & osmolality
• Distribute body water between
compartments
• Regulate acid-base balance
Electrolyte Imbalances
Sodium Imbalances

• Most abundant electrolyte in the ECF

• 135 to 145 mEq/L (135-145 mmol/L)
• Primary determinant of ECF volume and
osmolarity
• Regulated by: ADH, thirst, RAAS
• Loss or gain is accompanied by a loss or gain
of water
• Establish the electromechanical state
necessary for muscle contraction and
transmission of nerve impulses
• Daily requirement: min. 2 gm/day
Sodium Deficit (Hyponatremia)

Serum Na level of less

than 135 mEq/L
Pathophysiology

• Primarily occurs due to imbalance of water

rather than sodium
• Urine sodium assists in differentiating renal
from non-renal causes of hyponatremia
A. Non-renal fluid loss (i.e. vomiting,
diarrhea, sweating)
• Kidneys retain sodium → low urine
sodium
B. Renal Salt wasting (i.e. use of diuretics)
• High urine sodium concentration
Pathophysiology

• Dilutional hyponatremia
– ECF volume increased without any
edema
• Adrenal Insufficiency: aldosterone
deficiency
• Medications: anticonvulsants (i.e.
carbamazipine [Tegretol],
levetiracetam[(Keppra] and SSRI
(fluoxetine [Sarafem], sertraline [Zoloft])
• SIADH
Hyponatremia: PATHOPHYSIOLOGY

Decrease extracellular sodium level

↓
Increased concentration of cellular fluid
↓
Water pulled into the cells
↓
Cells swell
Hyponatremia: CLINICAL
MANIFESTATIONS
• Poor skin turgor, Dry mucosa
• Headache, Orthostatic hypotension
• N & V, abdominal cramps, Decreased
saliva production
• dilutional hyponatremia: anorexia,
muscle cramps, feeling of exhaustion
Clinical Manifestations

CNS: altered mental status, status epilepticus,

and coma
• Rationale: cellular swelling and cerebral
edema
– Acute hyponatremia: developing in less
than 48 hours
• i.e. brain herniation and compression of
midbrain structures
– Chronic Hyponatremia: developing over 48
hours or more
• i.e. status epilepticus
CNS con’t:
• serum Na < 115 mEq/L: ↑ ICP ( lethargy,
confusion, muscle twitching, focal weakness,
hemiparesis, papilledema, seizures, and
death may occur
Assessment and Diagnostic Findings

• Hx and PE (focused on neurologic

examinations)
• laboratory test results
– SIADH: serum Na < 100 mEq/L; urinary
sodium >20 mEq/L; urine specific gravity:
>1.012
– Decreased serum osmolality (except in
azotemia)
Assessment and Diagnostic Findings

– Hyponatremia primarily due to sodium loss:

• urine sodium content <20 mEq/L
• low urine specific gravity (1.002 to
1.004)
Medical Management

1. Sodium Replacement
• Oral sodium replacement from normal diet
• I.V. : lactated Ringer’s solution or isotonic
saline (0.9% NaCl)
• Serum sodium must not exceed > 12mEq/L
in 24 hours
– To avoid neurologic damage due to osmotic
demyelination with overcorrection (exceeding 140
mEq/L)
Medical Management

1. Sodium Replacement con’t

• SIADH
– Lithium (Eskalith) or demeclocycline (Declomycin):
antagonize the osmotic effect of ADH on the
medullary collecting tubule
Medical Management

2.Water Restriction
• For patient swith normal or excess fluid
volume: restricting fluid to a total of 800 mL in
24 hours
• neurologic symptoms are present: hypertonic
sodium solution (3% or 5% sodium chloride)
• edema alone: sodium is restricted
• edema and hyponatremia: sodium and water
are restricted
Medical Management

3. Pharmacologic Mgmt
• AVP receptor antagonist: stimulate free
water excretion
• IV conivaptan HCL (Vaprisol): moderate
to severe symptomatic hyponatremia
– non-peptide dual arginine vasopressin (AVP) V1A
and V2 receptor antagonist.
– inhibit the effects of AVP, also known as
antidiuretic hormone, on receptors in the kidneys
– C/I: seizures, delirium, or coma
•
Nursing Management
 1. DETECTING AND CONTROLLING
HYPONATREMIA

• Monitor I&O, weight

• Abnormal losses of Na who can consume
a general diet:
– encourages foods and fluids with a high
sodium content
– I.V. parenteral fluids
• Primary problem is water retention
– Restrict fluid intake
1. DETECTING AND CONTROLLING
HYPONATREMIA
• Patient taking Lithium: observe for
Lithium toxicity (loss of Na by abnormal
routes)
– Supplemental salt and fluid; avoid use
of diuretics
• Avoid excess water supplements
2. Evaluate fluid I&O, urine specific
gravity, and serum sodium levels
Serum sodium level > 145mEQ/L
Gain of sodium in excess of water or loss of
water in excess of sodium

SODIUM EXCESS
(HYPERNATREMIA)
Pathophysiology

• Risk factors: fluid deprivation in

unconscious pt., very old, very young,
and cognitively impaired pt
• Administration of hypertonic enteral
feedings without adequate water
supplements
• Insensible water loss (i.e.
hyperventilation, burns)
Pathophysiology

• DI
• Less common causes: heat stroke, near
drowning in sea water, and malfunction
of hemodialysis or peritoneal dialysis
systems, IV adm. of hypertonic saline,
excessive use of sodium bicarbonate
Pathophysiology

Increased serum sodium concentration

↓
Fluid pulled out of the cells
↓
Cells shrink: cellular dehydration
Clinical Manifestations

• Primarily neurologic
– Moderate hypernatremia:
restlessness and weakness
– Severe hypernatremia: disorientation,
delusions, and hallucinations,
possible permanent brain damage
(due to hemorrhages that result from
brain contraction)
Clinical Manifestations

• Thirst: primary characteristics of

hypernatremia
• Other signs: dry, swollen tongue and
sticky mucous membranes; flushed
skin; peripheral and pulmonary edema;
postural hypotension; oliguria;
increased muscle tone and deep tendon
reflexes; mild increase in temp
Assessment and Diagnostic Findings

• Serum Na > 145 mEq/L and serum

osmolality >300 mOsm/kg
• Increased urine specific gravity and
urine osmolality: kidneys attempt to
conserve water
• DI: diluted urine; urine osmolality <
250mOsm/kg
Medical Management

• IV infusion:
– hypotonic electrolyte solution (e.g.
0.3% NaCl)
• safer: allows gradual reduction in
serum sodium → decreasing risk of
cerebral edema
– isotonic non saline solution (D5W):
water replacement without sodium
Medical Management

• Serum sodium reduced at a rate of 0.5 – 1

mEq/L/h: allow sufficient time for
readjustment thru diffusion across fluid
compartments
• For DI: Desmopressin acetate (DDAVP)
• Diuretics
• Dialysis
Nursing management

• Preventing Hypernatremia
✓ Provide fluids at regular intervals: esp. debilitated
and unconscious patients
✓ Enteral feedings or parenteral route: alternative
route for intake
✓ diabetes insipidus: Adequate fluid intake
• Correcting Hypernatremia
✓ Done gradually
✓ Monitor pt.’s response to the fluids: review serial
serum sodium and observe changes in neurologic
signs.
Potassium Imbalances
• Potassium: major intracellular electrolyte ; 98%
inside the cells, 2% in ECF
• Important in neuromuscular function; skeletal
and cardiac muscle activity
• Normal serum potassium: 3.5 – 5 mEq/L
• Kidneys regulate potassium balance
• K deficit → alkalosis
• K excess → acidosis
• Anabolism (glycogenesis): K enters cells
• Catabolism (trauma, dehydration, starvation): K
leaves the cells
✓Serum k < 3.5 mEq/L
✓Occurs with Alkalosis: shift of serum
K into the cells

POTASSIUM DEFICIT
(HYPOKALEMIA)
Pathophysiology

• Meds
– Potassium loosing diuretics: thiazides and
loop
– Corticostreroids, sodium penicillin,
carbenicillin, and amphotericin B
• GI losses: vomiting and gastric suction;
diarrhea, prolonged intestinal suction, recent
ileostomy, and vilous adenoma (tumor of the
intestinal tract characterized by excretion of
potassium rich mucus)
Pathophysiology

• Alterations in acid-base balance: Alkalosis

– Shifting of potassium inside the cells;
shifting of hydrogen ions outside the cells=
correct ph
• Hyperaldosteronism: renal potassium wasting
– Primary: adrenal adenomas
– Secondary: cirrhosis, nephrotic syndrome,
heart failure, or malignant hypertension
Pathophysiology

• Insulin hypersecretion: secondary to high

carbohydrate parenteral nutrition
– Insulin promotes entry of potassium into
skeletal muscle and hepatic cells
• Patients who do not eat a normal diet for a
prolonged period of time
– Debilitated elderly, pt w/ alcoholism, pt.
w/anorexia nervosa
– Pt w/ bulimia; misuse of laxatives, diuretics,
and enema
Pathophysiology

• Decreased K+ levels in ECF will require

greater than normal stimulus for
depolarization of the membrane in order to
initiate action potential
• Almost all manifestations that occur with
hypokalemia result from slowed neuronal
excitability and its consequent effects on
muscle function.
Clinical Manifestations

• Clinical sxs develop if serum k < 3 mEq/L

1. GI manifestations dt slowed muscle
contraction- anorexia, abdominal distention,
constipation, vomiting, ileus
2. Slowed skeletal muscle contraction leads to
muscle weakness, leg cramps, paralysis
3. Neurologic manifestations- fatigue,
paresthesias, hyporeflexia, and irritability
Clinical Manifestations

• Cardiac manifestations- Dysrrhythmias,

decreased myocardial contraction
(manifested by hypotension and slow,
weakened pulse), < 2.5meq/L=
ventricular fibrillation and cardiac arrest
• Pulmonary manifestations- shallow
respirations, SOB, apnea leading to
respiratory arrest
• Neurologic manifestations- dysphasia,
confusion, depression, convulsions,
areflexia, and coma
• Renal- polyuria, nocturia, ↓plasma
osmolality
Assessment and Diagnostic Findings

1. ECG:
– flat T waves or inverted T waves:
suggesting ischemia
– depressed ST segment
– elevated U wave: specific to
hypokalemia
Assessment and Diagnostic Findings

2. increased risk to digitalis toxicity:

increased sensitivity to digitalis
3. Metabolic alkalosis
4. 24 hour urinary potassium excretion
test: distinguish between renal and
extrarenal loss
Medical Management

• Restore Potassium levels- 40-60 meg/day in

IV solution
• Mild to moderate hypokalemia- correct or
control the cause of loss by supplementing
K+ intake via diet or with meds.
Medical Management

• Diet containing sufficient potassium: 50-100

mEq/day (ave. adult)
– Ex. vegetables, legumes, whole grains,
milk, and meat
• Fruits: Banana, dried fruits
(raisins,prunes), orange, raw carrots,
raw tomato, baked potato, melon
(cantaloupe), watermelon
Medical Management

• Oral K+ supplemet- mild hypokalemia

(3.3-3.5 meq/L)
– Ng resp: take with meals, glass of
H20 or with juice
 Medical Management

• IV potassium supplement
– Severe hypokalemia (serum level 2 mEq/L)
– 10 – 20 meq/L can be given every hour if
diluted in IV
• Ng resp: Give IV K+ diluted in IV fluid
(20-40 meq/L).Must not be given IM,
Never given as Bolus (IV Push) injection
• May use saline as diluent, not dextrose
• Cardiac monitor (safety)
• Large veins must be used for
concentrations > 20-40 meq/L
Nursing Management:

1. Assess: risk factors, hx on dietary intake,

conditions that promote K+ loss(diuretics,
OTC meds), PE
• Assess cardiac function and renal function-
hourly in severe cases, progress to q8H as
condition progress.
• Monitor blood levels of ct taking digitalis;
monitor signs of digitalis toxicity
Nursing Management:

2. Interventions:
• Give oral or IV K+, ensuring it is diluted
• Always agitate IV bag containing K+ before
hanging. Use Infusion pump if available
• Monitor IV sites for phlebitis hourly and
change IV sites every 72 H; d/c IV if pain or
tenderness is felt in IV site
• Report UO <0.5 ml/kg/hr for 2 consecutive
hours, if pulse deficit > 20 bpm, signs of
impaired peripheral tse. Perfusion
Nursing Management:

2. Interventions
• Report cardiac dysrrhythmias of increasing
severity.
• Employ safety and seizure precaution, bed in
low position, with padded side rails up
• Encourage ct. to consume foods high in K+;
teach ct that prolonged cooking of vegetables
may result in wasting of essential nutrients
instead, suggest steaming and raw veg.
Nursing Management:

• Take K+ supplements with meals, glass of

H20, or juice
• Instruct ct to take 30-60 ml/ hr of fluids with
electrolytes
• Avoid OTC especially laxatives without
approval from physician
 ✓> 5.0 mEq/L
✓Cause: iatrotrogenic (treatment induce)
✓Associated with cardiac arrest

POTASSIUM EXCESS
(HYPERKALEMIA)
Pathophysiology

3 major causes:
1. decreased renal excretion of K
• Untreated renal failure, result of infection,
excessive intake in food or medications
(potassium chloride, heparin, ACE-inhibitors)
• Addison’s disease: deficient adrenal
hormones
2. rapid administration of K
3. movement of K from the ICF compartment to
the ECF compartment
• Acidosis→ buffer ph in the ECF
Pathophysiology

• Increased level of Serum K results in

depolarization of membrane potential of cells
• Resulting in the opening of voltage-gated
sodium channels, but not enough to generate
action potential
• The open Sodium channels inactivate and
become refractory
• This increased the threshold to generate
action potential
• This leads to impairment of neuromuscular,
cardiac, GI systems
Clinical Manifestations

• Mild to Moderate (K+ nearly 6meq/L)- nerve

and muscle irritability resulting in paresthesia,
tachycardia, intestinal colic, diarrhea.
• As K+ approaches 7meq/L- disturbances in
nerve and muscle function develops.
– Impaired cardiac conduction &ventricular
contractions
– Hypotension
– Cardiac arrest
– Convulsion
– Severe neuromuscular weakness progressing to
flaccid paralysis; respiratory ,muscle paralysis
•
Clinical Manifestations

• Cardiac effects: if serum level ≥8 mEq/L

– Earliest (> 6mEq/L): peak, narrow T waves;
ST segment depression; shortened QT
interval
– Cont. increase in serum K: prolonged PR
interval → disappearance of P waves →
widening of QRS complex
Clinical
Manifestations
Assessment & Dx Findings

• Se K+ level > 5meq/L

• BUN, Se Creatinine
• ABG analysis
• ECG changes:
– > 5.5 meq/L- Tall, peaked T wave
and shallow U wave
– > 7.0 meq/L- Narrow, peaked T wave
and QRS widening
Medical Management

• Non-acute: restrict dietary K and K-containing

medications
• Severe hyper K: cation exchange resins (e.g.
sodium polystyrene sulfonate [Kayexalate])
– Use in pt w/ renal impairment; C/I in pt. w/
paralytic ileus
– s/e: hypomagnesemia, hypocalcemia,
sodium retention and fluid overload
 Medical Management

• Emergency pharmacologic Therapy

– IV Ca Gluconate: antagonizes the action of
hyperkalemia on the heart
• Monitor blood pressure: hypotension
• Monitor ECG: stop infusion if bradycardia
is present
• Extra caution if the pt has been
“digitalized”: parenteral Ca may precipitate
digitalis toxicity
Medical Management

• Emergency pharmacologic Therapy

– IV sodium bicarbonate: alkalinize plasma
• Temp. shift of potassium into the cells;
antagonize the cardiac effects of
potassium
– IV adm. Of regular insulin &
hypertonic dextrose solution: temp.
shift of K into the cells
Medical Management

• Emergency pharmacologic Therapy

– Loop diuretics: furosemide (Lasix)
• Inhibit reabsorption of Na, K, Cl
– Beta-2 agonist: albuterol (Ventolin)
• Decrease K (move K inside the cells);
used in the absence of ischemic heart
disease (may cause tachycardia and
chest discomforts)
Nursing Management

1. Preventing Hyperkalemia
• Adhere to prescribe potassium restriction:
avoid potassium rich foods
2. Correcting Hyperkalemia
• Administer and monitor potassium solutions
closely
• Caution pt. to use salt substitute sparingly or
other supplementary forms of potassium or
potassium-converting diuretics
•
CALCIUM IMBALANCES
• >99% located in the skeletal system
• Small amt. located outside the bone
circulates in the serum: Total serum Ca (8.6
to 10.2 mg/dl [2.2 to 2.6 mmol/L])
– Protein bound: primarily albumin
– Partly ionized (50%): normal 4.5 to 5.1
mg/dl (1.1 to 1.3 mmol/L)
– Complexed: combined w/ non-protein
anions (phosphate, citrate, and carbonate)
Functions:

– Transmission of nerve impulses

– Helps regulate muscle contraction
and relaxation
– Instrumental in activating enzymes
that stimulate many essential
chemical reactions
– Plays a role in blood coagulation
• Serum Ca level controlled by PTH and
calcitonin
Free ionized Ca is needed for:

• Blood coagulation
• Smooth, skeletal and cardiac muscle
function
• Nerve function
• Bone and teeth formation
Calcium Deficit (Hypocalcemia)

Serum values
<8.6mg/dl [2.15
mmol/L]
Collaborative mgmt

• Monitor breathing
• Ca gluconate
• High Ca diet
• Oral Ca salts: Ca gluconate, Ca
chloride, and Ca gluceptate
• Vit. D & PTH supplements
• Phosphate-binder (AL-OH)
• Safety precautions: seizures
Acute symptomatic: IV Ca salt (Ca gluconate,
Ca chloride, and Ca gluceptate)
• Avoid rapod adm: may cause cardiac arrest
• can cause digitalis toxicity: calcium ions exert
an effect similar to that of
• digitalis
• IV calcium should be diluted in D5W and
given as a slow IV bolus or a slow IV infusion
• IV site must be observed often for any
evidence of infiltration because of the risk for
sloughing of tissues
 CALCIUM EXCESS
(HYPERCALCEMIA)

Serum Ca > 10.2 mg/dl

(2.6 mmol/L
Magnesium Imbalances
• Most abundant intracellular cation after
potassium
• Activator of many intracellular enzymes; plays
a role in carbohydrate and protein
metabolism
• Normal serum mg: 1.3 – 2.3 mg/dl (0.62 –
0.95 mmol/L)
• 1/3 bound to protein; 2/3 free cations
• important in neuromuscular function: affects
neuromuscular irritability and contractility
• Mg excess ⇢ decreased neuromuscular
excitability ( has a sedative effect on
neuromuscular junction, increases threshold
in nerve fibers
• Mg deficit ⇢ increased neuromuscular
irritability
• CV: acts peripherally to produce vasodilation
& decreased peripheral resistance
• Found in: bone & soft tissues
 Magnesium Deficit
(Hypomagnesemia)

✓Serum mg concentration <1.3

mg/dl (0.62 mmol/L)
✓Frequently associated w/
hypokalemia and hypocalcemia
• Of the ct with Ca, Na, K imbalance, 22-
42% has Mg imbalance
• Rare imbalance in ct who consume well
balanced diet
• Becoming recognized as a common
cause of refractory hypokalemia and
hypocalcemia
Pathophysiology

• Loss of Mg from GI tract: NG suction,

diarrhea, fistulas, disruption of small-
bowel function (e.g. intestinal resection
or inflammatory bowel disease)
– Fluid from lower GI tract has high
concentration of Mg
• Alcoholism: may occur w/ alcohol
withdrawal
• intracellular shift of Mg associated w/ IV
glucose adm.
Pathophysiology

• Enteral and parenteral feedings

deficient in magnesium
• Others: aminoglycosides, cyclosporine,
cisplatin, diuretics, digitalis,
amphotericin
• rapid administration of citrated blood
• DKA: increased renal excretion
secondary to osmotic diuresis & shifting
of Mg into the cells w/ insulin therapy
Clinical Manifestations

• Symptoms occur if serum level < 1mEq/L

• Neuromuscular changes:
– Hyperexcitability w/ muscle weakness,
tremors, & athetoid movements (slow,
involuntary twisting and writhing)
• Others: w/ accompanying hypocalcemia
– Tetany, nystagmus, vertigo, generalized
tonic-clonic or focal seizures, laryngeal
stridor, and positive Chvosteks’s and
Trousseau’s signs
 Clinical Manifestations
• Alterations in mood
– Apathy, depression, apprehension, and
extreme agitation, ataxia, dizziness,
insomnia, confusion
– Delirium, auditory and visual hallucinations,
and frank psychosis may occur
• ECG
– Prolonged QRS, depressed ST segment,
predisposed to PVCs, SVT, torsades de
pointes, and VFib
• Increased susceptibility to digitalis toxicity
Assessment and Dx Findings

1. serum mg level < 1.3 mEq/dL or 0.62

mmol/L
2. urine magnesium level: determine the
cause
3. nuclear magnetic resonance
spectroscopy & ion-selective electrode
– Direct means of measuring ionized
serum magnesium levels
Medical Management

• Mild deficiency:
– Diet: green leafy vegetables, nuts,
seeds, legumes, whole grains,
seafood, peanut butter, and cocoa
– Oral magnesium salts: S/E: diarrhea
Medical Management

• IV Magnesium sulfate: adm via infusion pump

– Rapid adm. Can lead to heart block or
asystole
– Monitor: V/S and urine output (refer if u.o.=
100ml over 4 hours) before, during, and
after adm.
– Prepare Ca gluconate: treat hypocalcemic
tetany and hypermagnesemia
Nursing Management

• Monitor pt. receiving digitalis

• Severe hypomagnesemia: seizure precaution
• If confusion observed: safety precaution
• Screened for dysphagia
• Health teaching given - magnesium deficit
from abuse of diuretic or laxatives
• Alcohol abuse: teaching, counseling, support,
and possible referral to alcohol abstinence
program or other professional help
Serum level >2.3 mg/dL (0.95 mmol/L);
rare

MAGNESIUM EXCESS
(HYPERMAGNESEMIA)
Pathophysiology

• Renal failure: most common cause

• Untreated DKA: catabolism → release of
cellular magnesium
– Cannot be excreted bec. Of fluid depletion
and oliguria
• Treatmen for PIHor low hypomagnesemia
• Addison’s disease, or hypothermia
Pathophysiology

• Excessive use of Magnesium-based antacids

(Maalox, Riopan, Mylanta) or laxatives (milk
of magnesia)
• Meds that decrease GI motility: opioids and
anticholinergics
• Lithium intoxication
• Excessive soft tissue injury or necrosis :
trauma, shock, sepsis, cardiac arrest, severe
burns
Clinical Manifestations

• Depress CNS and peripheral

neuromuscular junction
• Mild increase
– Lower BP: peripheral vasodilation
– Nausea and vomiting, weakness,
soft-tissue calcifications, facial
flushing, and sensations of warmth
Clinical Manifestations

• Higher concentration
– Lethargy, dysarthria, drowsiness
– Lost of DTRs, muscle weakness, and
paralysis
– Depressed respi center: serum level
exceeds 10 mEq/L
– Coma, AV heart block, cardiac arrest
– Platelet clumping and delayed thrombin
formation
Assessment and Dx findings

1. serum Mg level: >2.3 mEq/dL (0.95

mmol/L)
2. Hyperkalemia & hypercalcemia
3. ECG: prolonged PR interval, tall T
waves, widened QRS, prolonged QT
interval, AV block
Medical Management

• Avoid magnesium adm. to patients w/ renal

failure.
• Discontinue oral and parenteral magnesium
salts: severe hypermagnesemia
• IV Ca gluconate (antagonizes the
cardiovascular and neuromuscular effects of
magnesium) and Ventilatory support: for
respi. depression and defective cardiac
conduction
Medical Management

• Hemodialysis w/ magnesium free dialysate

• Loop diuretics and IV sodium chloride or
lactated ringer’s solution - to enhance
excretion
Nursing Management:

• Monitor V/S: note hypotension and

shallow respiration
• Observe decreased DTRs and changes
in LOC
• Avoid meds containing magnesium to
patients with renal failure
• Caution when preparing and
administering magnesium containing
fluids parenterally
•
THE END……..