ELECTROLYTE IMBALANCES

N201 MODULE 3.2

J. SAVOY
 LEARNING OBJECTIVES:
1. DIFFERENTIATE BETWEEN TYPES OF ELECTROLYTE IMBALANCES:
SODIUM, POTASSIUM, CALCIUM.
2. INTERPRET PATIENT HISTORY, ASSESSMENT DATA, AND DIAGNOSTIC
TESTS IN RELATION TO FLUID AND ELECTROLYTE IMBALANCE IN A POST-
OPERATIVE PATIENT.
3. APPLY THE NURSING PROCESS TO A PATIENT WITH AN ELECTROLYTE
IMBALANCE.
4. ANALYZE METHODS OF MANAGING ELECTROLYTE IMBALANCES IN
THE SURGICAL PATIENT.
 FLUID COMPARTMENTS
INTRACELLULAR FLUID (ICF)
EXTRACELLULAR FLUID (ECF)
1. INTRAVASCULAR (PLASMA) – 1/3 OF ECF
2. INTERSTITIAL- 2/3’S OF ECF
3. TRANSCELLULAR – CSF, GI, PLEURAL, SYNOVIAL
 SODIUM

IMBALANCES TYPICALLY ASSOCIATED WITH PARALLEL

CHANGES IN OSMOLALITY
PLAYS A MAJOR ROLE IN -
1. ECF VOLUME AND CONCENTRATION
2. GENERATION AND TRANSMISSION OF NERVE
IMPULSES
3. REGULATION OF ACID-BASE BALANCE
 SODIUM (NA)

• ABSORBED FROM FOOD IN GI TRACT

• KIDNEYS ARE PRIMARY REGULATOR OF SODIUM
BALANCE
• NA LEAVES THE BODY THROUGH:
• URINE
• SWEAT
• FECES
 THE KIDNEYS ARE THE PRIMARY REGULATOR
OF SODIUM BALANCE

• ANTIDIURETIC HORMONE (ADH) REGULATION:

• EXCRETING OR RETAINING WATER
• ALDOSTERONE REGULATION:
• PROMOTING NA REABSORPTION FROM RENAL TUBULES

SERUM SODIUM LEVEL REFLECTS RATIO OF NA TO H2O

• THUS CHANGES MAY REFLECT A WATER IMBALANCE, NA
IMBALANCE OR COMBINATION OF THE TWO.
 DECREASED SODIUM- HYPONATREMIA
RESULTS FROM:
1. LOSS OF SODIUM-CONTAINING FLUIDS (ISOTONIC LOSS)
2. GAIN OF WATER IN ECF (DILUTIONAL LOW SODIUM).

HYPONATREMIA CAUSES EXTRACELLULAR HYPO-OSMOLALITY WITH A

SHIFT OF WATER INTO THE CELLS (TO CORRECT THE PROBLEM)

NORMAL SERUM SODIUM: 136-145 MMOL/L (ADULT)

• HYPONATREMIA = SERUM SODIUM LEVEL <135MEQ/L
• CRITICAL VALUES <120 MMOL/L OR >160 MMOL/L
 HYPONATREMIA IN THE SURGICAL PATIENT:

CLINICAL INDICATORS AND TREATMENT DEPEND ON THE

CAUSE!
IS THE HYPONATREMIA R/T:
A. NORMAL
B. DECREASED
C. OR INCREASED ECF VOLUME?
IF LOSS OF SODIUM IS WITHOUT A LOSS OF FLUID; RESULT IS ↓
OSMOLALITY OF ECF.
 HYPONATREMIA-
MOST LIKELY CAUSES IN THE SURGICAL PATIENT:

1. TEMPORARY INCREASE IN VASOPRESSIN (ADH) RELEASE

AFTER ANESTHESIA AND THE STRESS OF SURGERY (STRESS
RESPONSE)
2. IV FLUIDS – IMPACT ON ELECTROLYTES?
2. GI WOUND DRAINAGE/LOSS-
• VOMITING
• DIARRHEA
• NASOGASTRIC SUCTION
 HYPONATREMIA- CAUSES CONT’D:

3. DIURETIC USE
4. RENAL DISEASE
• KIDNEY DISEASE RESULTING IN SALT WASTING
• ADRENAL INSUFFICIENCY
5. WATER EXCESS – DILUTIONAL HYPONATREMIA
6. HYPERGLYCEMIA
7. USE OF SODIUM FREE OR HYPOTONIC IV FLUIDS?
 MANIFESTATIONS OF HYPONATREMIA :
ON PHYSICAL EXAM-
SYMPTOMS ARE RELATED TO CELLULAR SWELLING

• SERUM SODIUM LEVEL< 135 • NAUSEA & VOMITING

MMOL/L
• DIARRHEA
• APPREHENSION, IRRITABILITY,
• DRY MUCOUS MEMBRANES
CONFUSION
• POSTURAL HYPOTENSION • SEIZURES, TREMORS

• TACHYCARDIA; RAPID THREAD • COMA

PULSE
 HYPONATREMIA
NURSING DIAGNOSES

• RISK FOR INJURY

• RISK FOR ELECTROLYTE IMBALANCE
• POTENTIAL COMPLICATION: SEVERE NEUROLOGICAL
CHANGES
• MAY BE R/T FLUID VOLUME DEFICIT (ISOTONIC LOSS)
THUS:
• DECREASED PERFUSION/CO - R/T LOW VOLUME…
 NURSING INTERVENTIONS HYPONATREMIA:
BASED ON ASSESSMENT FINDINGS:
1. CAUSED BY ABNORMAL FLUID LOSS
• FLUID REPLACEMENT WITH SODIUM-CONTAINING
SOLUTION
• LACTATED RINGERS
• ISOTONIC NACL
• BLOOD
• GOAL IS TO REPLACE BOTH WATER AND ELECTROLYTES
2. CAUSED BY FLUID EXCESS
• FLUID RESTRICTION
• DIURESIS
 ELEVATED SODIUM IN ECF -
HYPERNATREMIA
RESULTS FROM:
• ELEVATED SERUM SODIUM OCCURRING WITH WATER LOSS
OR SODIUM GAIN
• HYPERNATREMIA CAUSES HYPEROSMOLALITY
• SHIFT OF WATER OUT OF CELLS
• LEADING TO CELLULAR DEHYDRATION

LABORATORY FINDINGS: SERUM SODIUM LEVELS

>145MMOL/L
 HYPERNATREMIA CONT’D-

• PRIMARY PROTECTION IS STIMULATION OF THIRST

CENTER IN HYPOTHALAMUS.
• BODY ATTEMPTS TO CONSERVE WATER THROUGH RENAL
ABSORPTION
 HYPERNATREMIA IN THE SURGICAL PATIENT
POSSIBLE CAUSES: WATER LOSS OR SODIUM GAIN?
1. HYPERNATREMIA SECONDARY TO WATER DEFICIENCY?
• IMPAIRED LOC
• UNABLE TO ACCESS WATER
• IMPAIRED SENSE OF THIRST
• UNABLE TO SWALLOW
2. EXCESSIVE IV ADMINISTRATION OF HYPERTONIC SALINE
3. USE OF SODIUM-CONTAINING DRUGS
 MANIFESTATIONS OF HYPERNATREMIA :

DETERMINE THE CAUSE? VOLUME DEFICIT OR SODIUM GAIN?

• EXTREME THIRST
• FEVER
• DRY & FLUSHED SKIN
• DRY & STICKY TONGUE & MUCOUS MEMBRANES
• IMPAIRED LOC
• AGITATION, RESTLESSNESS, IRRITABILITY
• LETHARGY
• POSTURAL HYPOTENSION (IF WATER LOSS)
• SEIZURES AND COMA
 HYPERNATREMIA
NURSING DIAGNOSES

• RISK FOR INJURY

• RISK FOR ELECTROLYTE IMBALANCE
• POTENTIAL COMPLICATION: SEIZURES AND COMA
LEADING TO IRREVERSIBLE BRAIN DAMAGE
 HYPERNATREMIA
NURSING INTERVENTIONS
BASED ON ASSESSMENT FINDINGS:

• TREAT UNDERLYING CAUSE.

• IF ORAL FLUIDS CANNOT BE INGESTED -
• IV SOLUTION OF 5% DEXTROSE IN WATER OR HYPOTONIC
SALINE
• DIURETICS
• CAUTION IN CORRECTING; PATIENT MONITORING
IMBALANCES IN ECF VOLUME
 POTASSIUM
MAJOR ICF CATION
NECESSARY FOR:
• TRANSMISSION AND CONDUCTION OF NERVE AND MUSCLE
IMPULSES
• CELLULAR GROWTH
• MAINTENANCE OF CARDIAC RHYTHMS
• SKELETAL AND SMOOTH MUSCLE CONTRACTION
• ACID-BASE BALANCE
 POTASSIUM
SOURCE IS:
• DIET
• PARENTERAL – IV FLUIDS, STORED TRANSFUSED BLOOD,
POTASSIUM PENICILLIN
SERUM POTASSIUM LOSS:
• 90% ELIMINATED VIA THE KIDNEYS
• REMAINDER LOST IN STOOL AND SWEAT
• INVERSE RELATIONSHIP B/W NA AND K REABSORPTION IN KIDNEYS
• MAGNESIUM DEFICIENCY
• METABOLIC ALKALOSIS
 LOW POTASSIUM – HYPOKALEMIA
CAUSES:
ABNORMAL LOSSES OF K+
VIA THE KIDNEYS
OR GASTROINTESTINAL TRACT
DIARRHEA, VOMITING, ILEOSTOMY DRAINAGE
MAGNESIUM DEFICIENCY
METABOLIC ALKALOSIS
SURGERY – INCR CORTISOL, ADH

NORMAL SERUM POTASSIUM LEVEL 3.5-5.0 MMOL/L

 MANIFESTATIONS OF
HYPOKALEMIA-

1. MOST SERIOUS ARE CARDIAC

• LEAD TO LETHAL VENTRICULAR ARRHYTHMIAS
2. SKELETAL MUSCLE WEAKNESS (LEGS)
3. WEAKNESS OF RESPIRATORY MUSCLES
4. DECREASED GASTROINTESTINAL MOTILITY
5. IMPAIRED REGULATION OF ARTERIOLAR BLOOD FLOW
 HYPOKALEMIA
NURSING DIAGNOSES

• RISK FOR ELECTROLYTE IMBALANCE

• RISK FOR INJURY
• POTENTIAL COMPLICATION: DYSRHYTHMIAS
 NURSING INTERVENTIONS - HYPOKALEMIA
BASED ON ASSESSMENT FINDINGS:
INCREASE DIETARY INTAKE OF POTASSIUM
KCL SUPPLEMENTS ORALLY OR IV
SHOULD NOT EXCEED 10 TO 20 MEQ/HR
TO PREVENT HYPERKALEMIA AND CARDIAC ARREST
 ELEVATED POTASSIUM - HYPERKALEMIA

HIGH SERUM POTASSIUM CAUSED BY:

1. MASSIVE INTAKE
2. IMPAIRED RENAL EXCRETION
3. SHIFT FROM ICF TO ECF
4. MEDICATIONS
• DIURETICS
• ACE

MOST COMMON CAUSE IS RENAL FAILURE

 MANIFESTATIONS OF
HYPERKALEMIA
CRAMPING LEG PAIN
WEAK OR PARALYZED SKELETAL MUSCLES
VENTRICULAR FIBRILLATION OR CARDIAC STANDSTILL
ABDOMINAL CRAMPING OR DIARRHEA
 HYPERKALEMIA
NURSING DIAGNOSES

• RISK FOR ELECTROLYTE IMBALANCE

• RISK FOR INJURY
• POTENTIAL COMPLICATION: DYSRHYTHMIAS
 ECG EFFECTS OF HYPERKALEMIA

Copyright © 2014 Elsevier Canada, a division of Reed Elsevier Canada, Ltd.

 NURSING INTERVENTIONS - HYPERKALEMIA
BASED ON ASSESSMENT FINDINGS

1. ELIMINATE ORAL AND PARENTERAL K INTAKE.

2. INCREASE ELIMINATION OF K -
a) DIURETICS
b) KAYEXALATE
c) DIALYSIS
NURSING INTERVENTIONS - HYPERKALEMIA
BASED ON ASSESSMENT FINDINGS-
3. FORCE K+ FROM ECF TO ICF BY:
a) IV INSULIN OR SODIUM BICARBONATE (NACO3).
4. REVERSE MEMBRANE EFFECTS OF ELEVATED ECF
POTASSIUM BY:
b) ADMINISTERING CALCIUM GLUCONATE IV.
 CALCIUM
OBTAINED FROM INGESTED FOODS
MORE THAN 99% COMBINED WITH PHOSPHORUS AND
CONCENTRATED IN SKELETAL SYSTEM
INVERSE RELATIONSHIP WITH PHOSPHORUS
BONES ARE READILY AVAILABLE STORE
BLOCKS SODIUM TRANSPORT AND STABILIZES CELL
MEMBRANE
IONIZED FORM IS BIOLOGICALLY ACTIVE
 FUNCTIONS OF
CALCIUM

TRANSMISSION OF NERVE IMPULSES

MYOCARDIAL CONTRACTIONS
BLOOD CLOTTING
FORMATION OF TEETH AND BONE
MUSCLE CONTRACTIONS
 CALCIUM
NORMAL CALCIUM LEVEL –
TOTAL 2.25- 2.75 MMOL/L; 8.9-10.3 MG/DL
IONIZED 1.05-1.30 MMOL/L

BALANCE CONTROLLED BY:

• PARATHYROID HORMONE (PTH) - ↑ SERUM CA
• CALCITONIN – OPPOSES THE ACTION OF PTH
• VITAMIN D- CRITICAL IN PROCESS OF ↑ SERUM CA
 LOW CALCIUM - HYPOCALCEMIA
DEFINED AS TOTAL SERUM CALCIUM LEVEL < 8.9 MG/DL
CAUSES:
1. DECREASED PRODUCTION OF PTH
• PARATHYROIDECTOMY
• SURGERY OR INJURY TO THYROID
• IF PARATHYROID GLAND IS REMOVED OR DAMAGED
2. ACUTE PANCREATITIS
 OTHER CAUSES OF HYPOCALCEMIA:
3. ALKALOSIS
4. DECREASED INTAKE
5. LOW MAGNESIUM LEVEL
• CAN DECREASE PTH SECRETION
6. MALABSORPTION SYNDROMES
7. MULTIPLE BLOOD TRANSFUSIONS
8. VITAMIN D DEFICIENCY
9. MEDICATIONS – LOOP DIURETICS
 MANIFESTATIONS
OF HYPOCALCEMIA-

1. CARDIOVASCULAR
2. POSITIVE TROUSSEAU’S OR CHVOSTEK’S SIGN
3. LARYNGOSPASM AND STRIDOR
4. DYSPHAGIA
5. PARESTHESIA (TINGLING) AROUND THE MOUTH OR IN
THE EXTREMITIES
6. OSTEOPOROSIS
7. CONVULSIONS
 HYPOCALCEMIA
NURSING DIAGNOSES

• RISK FOR ELECTROLYTE IMBALANCE

• RISK FOR INJURY
• POTENTIAL COMPLICATION: FRACTURE OR RESPIRATORY
ARREST
 NURSING INTERVENTIONS - HYPOCALCEMIA
BASED ON ASSESSMENT FINDINGS:

TREAT UNDERLYING CAUSE.

1. ORAL OR IV CALCIUM SUPPLEMENTS
• IV CALCIUM IN ACUTE SYMPTOMATIC HYPOCALCEMIA
• NOT IM TO AVOID LOCAL REACTIONS
2. TREAT PAIN AND ANXIETY TO PREVENT
HYPERVENTILATION-
INDUCED RESPIRATORY ALKALOSIS.
TESTS FOR HYPOCALCEMIA

Copyright © 2014 Elsevier Canada, a division

of Reed Elsevier Canada, Ltd.
 HIGH CALCIUM – HYPERCALCEMIA

HIGH SERUM CALCIUM LEVELS CAUSED BY:

• HYPERPARATHYROIDISM (TWO-THIRDS OF CASES)
• MALIGNANCY
• BREAST, LUNG, MULTIPLE MYELOMA, LYMPHOMA
• VITAMIN D OVERDOSE
• PROLONGED IMMOBILIZATION
• THIAZIDE DIURETICS
 MANIFESTATIONS
OF HYPERCALCEMIA

1. IMPAIRMENT OF MEMORY
2. CONFUSION; BIZARRE BEHAVIOR
3. DISORIENTATION; INATTENTIVE
4. FATIGUE; LETHARGY, DROWSINESS
5. CONSTIPATION
6. BONE PAIN, FRACTURES
NURSING INTERVENTIONS - HYPERCALCEMIA
BASED ON ASSESSMENT FINDINGS-

TREAT UNDERLYING CAUSE:

1. PRIMARY HYPERPARATHYROIDISM – PARATHYROIDECTOMY
2. EXCRETION OF CA WITH LOOP DIURETIC
3. HYDRATION WITH ISOTONIC SALINE INFUSION
4. SYNTHETIC CALCITONIN
5. MOBILIZATION IF POSSIBLE
6. MALIGNANCY – REDUCE SERUM CALCIUM LEVELS
 HYPERCALCEMIA
NURSING DIAGNOSES

• RISK FOR ELECTROLYTE IMBALANCE

• RISK FOR INJURY
• POTENTIAL COMPLICATION: FRACTURE OR RESPIRATORY ARREST
 CREATININE

A WASTE PRODUCT PRODUCED BY PROTEIN BREAKDOWN

IS A MEASURE OF THE AMOUNT OF ACTIVE MUSCLE
TISSUE IN THE BODY
EXCRETED IN THE URINE
THE MOST ACCURATE INDICATOR OF RENAL FUNCTION;
CLOSELY APPROXIMATES GFR
NORMAL CR CLEARANCE VALUES; 1.42-2.25ML/SEC
 EGFR
THE AMOUNT OF BLOOD FILTERED BY THE GLOMERULI IN A GIVEN
TIME IS TERMED AS GLOMERULAR FILTRATION RATE (GFR)
NORMAL GFR IS ABOUT 125ML/MIN; ON AVERAGE, ONLY 1ML IS
EXCRETED AS URINE PER MINUTE AS THE CAPILLARY NETWORK
REABSORBS MOST GLOMERULAR FILTRATE BEFORE IT REACHES
THE END OF THE COLLECTING DUCT
 BRING YOUR PREP TO ELECTROLYTE CLASS

WELL DONE!
• HAS YOUR KNOWLEDGE OF F&E IMPROVED?
 COME TO CLASS PREPARED TO USE YOUR PREP IN
GROUP WORK FOR APPLICATION TO THE
SURGICAL PATIENT
 BRING YOUR LEWIS TEXT.
Electrolyte Function Cause Cause S&S of S&S of Nsg Nsg
of of HYPO HYPER Interventions Interventions
HYPO HYPER HYPO HYPER

Sodium
Na

Potassium
K+

Calcium
Ca