Seminar

On

FLUID AND ELECTOLYTE IMBALANCE

Submitted to Submitted by
Mrs Vaishali Taksande Ms. Zenia.R.C
Professor M.Sc. Nursing,
S.R.M.M. College of Nursing S.R.M.M. College of Nursing
General objective
At the end of the class the students will be able to gain knowledge regarding fluid and
electrolyte imbalance and develop positive attitude and apply their skill in teaching as well as
practical area.

Specific objective

1. What are the compositions of body fluid.

2. Which are the hormones that help in regulation of fluid balances

3. Which are the routes of gain and loss of fluid.

4. Define electrolyte imbalance

5. Enlist the sign and symptom of electrolyte imbalance.

6. Enlist the complications of electrolyte imbalance.

7. Describe each complication.

8. Explain nurses responsibilities.

FLUID AND ELECTOLYTE IMBALANCE

  Tonicity:-ability of all the salts to cause an osmotic driving force that promotes water
movement from one compartment to another
 Osmotic pressure:-amount of hydrostatic pressure needed to stop the flow of water by
osmosis
 Oncotic pressure:-pressure exerted by protiens
 Osmotic diuresis:-occurs when amount of urine output increases due to excretion of
substances such as glucose, mannitol, or contrast agents in the urine
 Filtration:-Movement of water and solutes from an area of high hydrostatic pressure to
an area of low hydrostatic pressure
 eg:-filtration in kidneys

ROUTES OF GAIN AND LOSSES

 Kidneys
 Skin
 Lungs
 GI tract

LABORATORY TESTS FOR EVALUATING FLUID STATUS

 OSMOLALITY:-measures the solute concentration pre kg in fluid

 Serum osmolality primarily reflects sodium concentration normal value is 280-

300mOsm/kg

 Urine osmolality is determined by urea, creatinine, uric acid. Normal value is 250-
900mOsm/kg

 Serum osmolality=Na+2=glucose/18+BUN/3

 OSMOLARITY:-Concentration of solutes per liter of solution

 URINE SPECIFIC GRAVITY:-Measures kidney’s ability to excrete or conserve water.

Normal value is 1.010-1.025

 BLOOD UREA NITROGEN:-made up of urea, an end product of protein metabolism.

Normal value is 10-20mg/dl
 LABORATORY TESTS FOR EVALUATING FLUID STATUS
 CREATININE:-end product of muscle metabolism
 More reliable indicator than BUN

 HEMATOCRIT:-males 44-52%
Females 39-47%
 URINE SODIUM VALUES:-50-220mEq/24hrs
FLUID VOLUME DISTURBANCES
 Extra cellular fluid volume deficit
 Intracellular fluid volume deficit
 Extra cellular fluid volume excess
 Intracellular fluid volume excess
 Third spacing of fluid

EXTRA CELLULAR FLUID VOLUME DEFICIT

 Commonly called dehydration, is a decrease in intravascular and interstitial fluids. Mild
ECFVD:-loss of 1-2L OR 2% of body weight. Moderate ECFVD:-loss of 3-5L OR 5%
body weight. Severe ECFVD: loss of 5-10L OR 8% of body weight

ETIOLOGY

1. Lack of fluid intake

 Cognitive and physical impairment

 Dysphagia or risk for aspiration

 Tube feeding

2.Impaired thirst mechanism

3.Excess fluid output
 Vomiting
 Diarrhea
 Fever
 Diaphoresis
 Hyperglycemia
 Gastrointestinal suction
 Burns
 Blood loss
 Hyperventilation
 Hyperthyroidism
 Decreased ADH secretion
 Diabetes insipidus
 Addison’s disease
 Diuretic phase of ARF
 Use of diuretics
 Third space fluid shift
 Elderly are more prone to fluid loss due to
 Decreased renal concentration of urine
 An altered ADH response
 An increase in body weight

PATHOPHYSIOLOGY :-
  If dehydration is not corrected
 Fluid is shifted from cells
 Salivary glands become less active
 Less fluid is available for temperature regulation
 Cerebral cells may bleed or go into spasm

TYPES OF ECFVD
 Hyperosmolar fluid volume deficit
 Isoosmolar fluid volume deficit
 Hypotonic fluid volume deficit

CLINICAL MANIFESTATIONS
 Cardiovascular
 Thready, increased pulse rate
 Decreased BP and orthostatic hypotension
 Decrease in CVP and PCWP
 Flat neck and hand veins
 Diminished peripheral pulses
 Respiratory
 Increased rate and depth of respiration
 Neuromuscular
 Decreased CNS activity
 Fever
 Apprehension
 Restlessness, headache
 Renal
 Decreased urinary output
 Increased specific gravity
 Urine osmolarity above1000mOsm/kg
 Integumentary
 Dry skin
 Poor turgor
 Dry mouth
 Gastrointestinal
 Decreased motility and diminished bowel sounds
 Constipation
 Thirst
 Geriatric considerations
 Skin turgor is less valid
 Manifestations of cellular dehydration
 Dry mucous membrane of mouth and eye
 Cracked lips and furrowed tongue
 Soft and sunken eyes
 Muscle weakness
 Feces become hard and decreased in number
  Manifestations in children
 Child may be thirsty and slightly irritable
 If fontanel is open may be depressed
 Eyes appear sunken
 Tongue and inner side of the cheek is dry
 Child passes urine at longer intervels

DIAGNOSTIC FINDINGS
 BUN creatinine ratio >20:1
 Hematocrit above 55%
 Hypokalemia with GI and renal losses
 Hyperkalemia with adrenal insufficiency
 Hyponatremia with increased thirst and ADH release
 Hypernatremia from increased insensible loss and diabetes insipidus
 Urine specific gravity >1.030
 Urine osmolality>450mOsm/kg
 Serum osmolality >295 mOsm/kg
 MEDICAL MANAGEMENT
 Depends upon acuteness and severity of fluid deficit

Goals:-
 Replace fluids and electrolytes that have been lost
 Correct the underlying problem
 Oral rehydration
 If thirst mechanism is intact and client can drink oral route is preffered
 ORS is quickly absorbed
 Avoid cola and caffeine
 Composition of reduced osmolarity ORS
 Sodium chloride :- 2.6gm/L
 Glucose, anhydrous:- 13.5gm/L
 Potassium chloride :- 1.5gm/L
 Trisodium citrate :- 2.9gm/L
 Total weight :- 20.5gm/L

Intravenous rehydration
 Isotonic ECFVD:-isotonic solution
 Hypertonic ECFVD:-hypotonic solution
 Hypotonic ECFVD:-hypertonic solution
 Intravenous water and electrolyte solutions

Isotonic solutions
 0.9% saline
 5%dextrose in water
 5%dextrose in 0.225% saline
 Lactated ringers solution
Hypotonic solutions
 0.45% saline
 Intravenous water and electrolyte solutions

Hypertonic solutions
 3% NaCl
 5%NaCl
 5%dextrose in lactated ringer’s solution
 5%dextrose in 0.45% saline
 5%dextrose in 0.9% saline
 10%dextrose in water
Colloid solutions
 Dextran 40 in NS
 Monitoring for complications
 Monitor
 CVP
 Pulmonary artery pressure
 Urine output
 Body weight
 Lab values

NURSING MANAGEMENT ASSESSMENT

 H/O fluid loss
 Vital signs
 Orthostatic hypotension
 Peripheral vein filling time
 Intake and output
 Lab values
 h/o chronic illness
 Lung sounds
 Weight and height
 Oral cavity
 Level of consciousness
 Skin turgor
 Fluid volume deficit related to insufficient fluid intake, vomiting , diarrhea or third space
fluid shift
 Restore oral fluid intake
 Give small amounts of fluids of choice
 Keep fluids fresh and within reach
 Use antiemetics if needed
 Begin with clear fluids, broth, gelatin then progress to full liquids
 Restore fluids by intravenous routes
  Administer IV fluids cautiously
 Use large IV gauge
 Use IV pump or mini-drop for infusion
 Monitor IV solutions, IV sites and client outcome hourly
 rapid fluid administration may result in overload
 Monitor for complications
 Assess for risk of tissue break down
 Assess lung sounds for crackles
 Monitor lab values
 Altered oral mucous membrane related to lack of oral intake
 Give oral care every 2-4hrly
 Rinse the clients mouth 1-2hrly
 Avoid mouth washes with alcohol base
 Artificial saliva may be used
 Risk for injury related to orthostatic hypotension
 Provide safety through step progression position changes

HEALTH TEACHING
 Avoid exercise during high heat and humidity
 Wear appropriate clothing
 Use more caution if obese
 Drink cool water before exercise
 Avoid rapid fluid replacement
 Use caution while taking medication that interfere with thermoregulation

INTRACELLULAR FLUID VOLUME DEFICIT

 In severe dehydration cells become dehydrated
 Most common compensatory sign is thirst and oliguria
 Cellular manifestations are due to dysfunction in cerebral cells
 Management is through fluid replacement and correction of underlying cause

EXTRACELLULAR FLUID VOLUME EXCESS

 It is fluid overload or fluid excess
 It can be hypervolemia or third spacing

ETIOLOGY
 Compromised regulation of fluid movement and excretion
 Excessive ingestion of fluids or foods containing sodium
 Increased ADH and aldosterone

PATHOPHYSIOLOGY
 ECFVE can occur through
 Fluid overload
 Decreased plasma and albumin
 Lymphatic obstruction
  Tissue injury
 Renal disorders
 Fluid overload
 Decreased serum and albumin
 Lymphatic obstruction
 Tissue injury

TYPES OF ECFVE
 Isotonic over hydration
 Hypertonic over hydration
 Hypotonic over hydration
 Isotonic over hydration
 Results from excessive fluid in the extracellular fluid compartment
 No fluid shift between extracellular and intracellular fluid compartment
 Caueses circulatory over load and interstitial edema
 Hypertonic over hydration
 Caused by excessive sodium intake
 Fluid is drawn from intracellular fluid compartment

CLINICAL MANIFESTATIONS
 Respiratory manifestations
 Cough, dyspnea
 Crackles
 Pallor
 Cyanosis
 Cardiovascular manifestations
 Systemic venous engorgement
 Peripheral vein filling time above 5sec
 Elevated BP,CVP,PCWP
 Edema and rapid weight gain

CLINICAL MANIFESTATIONS
 CNS manifestations
 Confusion
 Headache
 Lethargy
 Seizures
 Coma

DIAGNOSTIC FINDINGS
 Plasma osmolality <275 mOsm/kg
 Plasma Na<135 mEq/L
 Hematocrit<45%
 Specific gravity<1.010
 BUN<8mg/dl
 Chest x-ray may reveal pulmonary congestion
MEDICAL MANAGEMENT
 Restriction of sodium and fluids
 Pharmacologic therapy:-diuretics
 Hemodialysis or peritoneal dialysis in renal insufficiency
 Nutritional therapy
 Sodium restricted diet

NURSING MANAGEMENT
 Assessment
 Vital signs
 Breath sounds
 Sacrum and legs for pitting edema
 Jugular vein and hand veins for distension
 Compare I & O chart
 Weigh the client daily
 Monitor edema
 Lab values
 Fluid volume excess related to specific cause
 Reduce sodium and fluid intake
 Strict I&O charting
 Schedule oral medications at meal time
 Use minimal amount of water to dissolve crushed medications
 Give client ice chips
 Provide frequent oral care
 Provide low sodium diet
 Salt substitute can be used
 Mobilize fluids
 Administer diuretics as prescribed
 In case of dependent edema avoid long periods of standing and sit with legs elevated
 Reduce complications
 Elevate head of bed 30-45 degrees
 Give oxygen
 Provide frequent skin care

INTRACELLULAR FLUID VOLUME EXCESS

 Also known as water intoxication
 May result from water excess or solute deficit

ETIOLOGY
 Administration of excessive amounts of hypoosmolar solutions
 Excessive consumption of tap water with inadequate amount of nutrients
 SIADH
 Compulsive water consumption in organic psychiatric illness

PATHOPHYSIOLOGY
  Hypoosmolar fluids in the vessels

 Moves into region of high concentration

 Accumilation of fluid in cells

 Edema

CLINICAL MANIFESTATIONS
 Neurologic manifestations are secondary to increased ICP
 ICP syndromes progresses cephalocaudally
 Early signs are cortical, then pupillary changes occurs
 Changes in vital signs
DIAGNOSTIC FINDINGS
 Plasma sodium level <125mEq/L

 Decreased hematocrit

 No test to reflect cell fluid volume

 CT and MRI for identifying the underlying cause

MANAGEMENT
 Reduce increased ICP with steroids and osmotic diuretics
 If SIADH is impending risk administer iv fluids containing NaCl
 Perform neurologic checks
 Monitor I&O daily
 Provide safety measures
EXTRACELLULAR FLUID VOLUME SHIFT:THIRD SPACING
 A change in location of extracellular fluid between the intravascular and interstitial
spaces
 It may be of two types
 Vascular fluid shifts to interstitial spaces
 Interstitial fluid shifts to vascular spaces
 Fluid that shifts to interstitial spaces remains there is referred to third spacing
 Contd..
 Common sites of third spacing include
 Plural cavity

 Peritoneal cavity

 Pericardial sac
ETIOLOGY
 Increased capillary permeability
  Decreased serum protein levels

 obstruction of venous portion of capillary

 Non functional lymphatic drainage system

PATHOPHYSIOLOGY

 Tissue injury

 Release of histamine and bradykinin

 Increased capillary prmeability

 Movement of fluid and solutes into interstitial spaces

PATHOPHYSIOLOGY
 Two phases of fluid shifts are associated with tissue injury
 Fluid shift from vascular to interstitial spaces
 Fluid shift back from interstitial to vascular spaces
 Protein deficiency also leads to fluid shift

CLINICAL MANIFESTATIONS
 Similar to manifestations of hypovolemia
 Manifestations include
 Pallor, cold limbs
 Weak and rapid pulse
 Hypotension
 Oliguria
 Decreased level of consciousness
 No change in body weight
CLINICAL MANIFESTATIONS
 If fluids collects and obstructs an organ, nerve, or vessel other clinical manifestations
may arise

 When fluid returns to blood vessels manifestations of fluid overload occurs

MEDICAL MANAGEMENT
 Begins with determining the cause of fluid volume shift

 If because of pericarditis, pericardiocentesis can be done

 If because of bowel obstruction, paracentesis can be done

  If because of pleural effusion, pleural tapping should be done
 Replace fluids
 Isosmolar iv fluids

 Albumin to replace protein from trauma

 Fluid overload can occur by aggressive replacement

 Stabilize other problems

NURSING MANAGEMENT
 Assess vital signs
 Monitor IV fluid replacement
 If third spacing is in the abdomen, measure abdominal girth
 If a limb is involved measure limb circumference and peripheral pulses
 Monitor urine output
ELECTROLYTE IMBALANCES INTRODUCTION
 Electrolytes are substances found in the intracellular and extracellular fluid that
dissociates into electrically charged particle known as ions
 Ions that carry positive charge are called cations
 Ions that carry negative charge are called anions
 Principal cation in the extracellular fluid is potassium
 Principal cation in the intracellular fluid is sodium

ELECTROLYTE BALANCE
 Dietary intake
 Normally human ingest far more electrolytes than needed each day
 When food intake is restricted intake of electrolytes become a concern

ELECTROLYTE BALANCE
 Regulated output:-factors that govern the output of electrolytes are
 Aldosterone
 ADH
 ANP
 Vitamin D
 Calcitonin
 Insulin
 Epinephrine
 Weight bearing and stress

SODIUM IMBALANCES
 Normal sodium level:-135-145mEq/L
 Imbalance occurs when concentration increases or decreases
  Hyponatremia
 Hypernatremia
HYPONATREMIA
 Plasma sodium level below 135mEq/L

 Most common electrolyte disorder

TYPES
 Hypovolemic hyponatremia

 Euvolemic hyponatremia

 Hypervolemic hyponatremia

 Redistributive hyponatremia

ETIOLOGY
 Causes of Hypovolemic hyponatremia
 Diuretic use
 Diabetic glycosuria
 Aldosterone deficiency
 Intrinsic renal disease
 Vomiting, diarrhea
 Increased sweating
 Burns
 High volume iliostomy
 Cause of euvolemic hyponatremia
 SIADH
 Many cancers
 CNS disorders
 Causes of redistributive hyponatremia
 Hyperglycemia
 hyprlipidemia
 Causes of Hypervolemic hyponatremia
 CHF
 Cirrhosis of liver
 Nephrotic syndrome
 Acute and chronic renal failure
RISK FACTORS
 Athletes and outdoor laborers
 Altered thirst mechanism
 Attempt for rapid rehydration
 Older adults

PATHOPHYSIOLOGY
  Decreased sodium concentration in
 Hyposmolar ecf
 Shift of fluid to icf
 Cellular edema

CLINICAL MANIFESTATIONS
 Neurological manifestations
 Headache, apprehension
 Confusion
 Hallucination
 Behavioral changes
 Seizures

CLINICAL MANIFESTATIONS
 Cardiovascular manifestations
 Decrease in systolic and diastolic pressure
 Orthostatic hypotension
 Weak thready pulse
 Compensatory tachycardia
 Respiratory manifestations
 Crackles
 Tachypnea, dyspnea, orthopnea
 Alteration in respiratory pattern
CLINICAL MANIFESTATIONS
 GI manifestations
 Nausea, vomiting
 Hyperactive bowel sounds
 Abdominal cramping
 Diarrhea
 Other manifestations
 Dryness of skin, tongue and mucus membrane
 High risk for altered skin integrity
DIAGNOSTIC FINDINGS
 Serum sodium<135mEq/L
 Chloride level <98mEq/L
 Serum osmolality <275mOsm/kg
 Urinary sodium content <20mEq/L
MEDCIAL MANAGEMENT
 Sodium replacement
 Can be replaced by mouth, NG tube, or parenterally
 Intake of balanced diet is usually adequate for mild losses
 If serum sodium is below 125mEq/L iv replacement with isotonic saline or lactated
ringers solution
 Serum sodium should not increase more than 12mEq/L in 24hrs
MEDCIAL MANAGEMENT
  Rapid replacement of sodium will cause osmotic demyelination
 Furosemide is given iv to prevent fluid overload
 Demeclocycline is given in SIADH
 In case of excess fluid volume hyponatremia is treated by restricting fluid volume
NURSING MANAGEMENT ASSESSMENT
 Diet, medication history, OTC drugs
 Body weight
 Intake and output
 Peripheral vein filling time
 Vital signs
 Plasma Na levels
HYPERNATREMIA
 Plasma sodium level >145mEq/L
 Occurs in about 1% hospitalized clients
 Carries a high mortality rate

TYPES
 Hypovolemic Hypernatremia
 Euvolemic hypernatrmia
 Hypervolemic hypernatremia
ETIOLOGY
 Unconscious patients
 Hypertonic enteral feedings
 Diabetes insipidus
 Heat stroke
 Near drowning in sea water
 Malfunctioning of HD or PD proprtioning system
 IV use of hypertonic saline

PATHOPHYSIOLOGY
 In hypernatremia osmotic shift of water out of cells
 Cellular dehydration
 Brain develops idiogenic osmoles
 Decreased myocardial contractility
 Myocardial depolarization occurs very easily
 Suppresses the effect of ADH and aldosterone
CLINICAL MANIFESTATIONS
 Neurologic manifestations
 Restlessness and weakness(in moderate)
 Disorientation, delusion, hallucination
 Agitation, muscle weakness
 Brain damage due to SAH
 Muscle twitching
 Trmor
 Hyperreflexia
 Seizures
CLINICAL MANIFESTATIONS
 Cardiovascular manifestations
 Orthostatic hypotension in hypovolemic hyponatremia
 Hypertension
 Jugular venous distension
 Prolonged peripheral vein emptying
 Extra heart sound(s3gallop)
 Generalized weight gain and edema
 Dysrhythmia
 Pulmonary manifestations
 Crackles
 Dyspnea
 Pleural effusion
 Other manifestations
 Dry and flushed skin
 Swollen tongue
 Sticky mucus membrane
 Increasing thirst
 Fever
DIAGNOSTIC FINDINGS
 Serum sodium>145mEq/L
 Serum osmolality>295mOsm/L
 Increased urine osmolality and specific gravity
MEDICAL MANAGEMENT
 For client with mild manifestations give oral fluid replacement
 To decrease total body sodium and replace fluid loss give hypotonic electrolyte solution
 Replacement should be at the rate of 2mEq/L/hr
 Desmopressin acetate in case of diabetes insipidus
NURSING MANAGEMENT
 Assessment
 Diet and medication history
 Vital signs
 Peripheral vein filling time
 Intake and output
 Oral membrane and skin assessment
 Signs of altered mental status

POTASSIUM IMBALANCES
 Potassium regulate intracellular osmolality
 Promotes the transmission and conduction of nerve impulses
 Promotes enzyme action for cell metabolism
 Fosters acid-base balance
 Normal serum potassium is 3.5-5.5mEq/L
 Daily requirement is 40-60mEq/day
 90% of potassium is excreted through kidneys and remainder through feces
 Substances that can alter potassium levels are
  Insulin
 Glucagon
 Adrenocortical hormones
 Catecholamines
 Beta adrenergic agonists
 Alpha adrenergic agonists

HYPOKALEMIA
 Plasma potassium level <3.5mEq/L
 Common electrolyte disorder in elderly population
ETIOLOGY
 Inadequate potassium intake
 GI loss of potassium
 Alkalosis
 Hyperaldosteronism
 Potassium loosing diuretics
 Hyper secretion of insulin
 Magnesium and penicillin causes renal potassium loss

PATHOPHYSIOLOGY
 Decreased plasma k level

 Decrease in potassium gradient

 Increased resting membrane potential

 Increased excitability

 More response to stimuli

CLINICAL MANIFESTATIONS
 Anorexia, abdominal distension
 Constipation
 Muscle weakness and flabbiness
 Leg cramps
 Fatigue
 Parasthesias
 Hyporeflexia
 Irritability
 ECG changes
 Hypotension
 Slow weakened pulse
 Shortness of breath
 Deterioration of respiratory muscle contraction
DIAGNOSTIC FINDINGS
 Plasma potassium <3.5mEq/l
 ECG changes
 Renal potassium excretion>20mEq/L
MEDICAL MANAGEMENT
 Maintenance dose of potassium is 40-60mEq/L
 For mild to moderate hypokalemia supplement potassium through diet or oral
medications
 Give oral potassium with a glass of water, juice, or with milk
 Severe hypokalemia requires IV intervention
 If the potassium level is between 3-3.4mEq/L, 100-200mEq of potassium is needed
 If it is below 3mEq/L 200-400 mEq/L is needed
 If hypokalemia is refractory to treatment assess for hypomagnesemia
NURSING MANAGEMENT
 Assessment
 Diet and medication history
 Lab reports
 Use of general anesthesia
 NPO status
 Cardiac function
 Renal function
 Neuromuscular and bowel function
HYPERKALEMIA
 Elevation of potassium level >5mEq/L
 Rare in clients with normal renal function
 More in people with acute renal failure
ETIOLOGY
 Retention of potassium by the body
 Excessive release of potassium by the cells
 Excessive infusion of IV solutions or excessive oral intake
 The underlying cause is often related to kidney function
 Tumor lysis syndrome
 Burns, crush injuries and severe infections
 Stored blood
 Open heart surgery
 Potassium sparing diuretics
 ACE inhibitors
 Adrenal insufficiency
 Acidosis
PATHOPHYSIOLOGY
 Hyperkalemia increases cell membranes excitation threshold
 Cells become less excitable
 Muscles become weak, flaccid and paralyzed

CLINICAL MANIFESTATIONS
  Mild to moderate Hyperkalemia can cause nerve and muscle irritability resulting in
 Paresthesia
 Tachycardia
 Intestinal colic
 Dairrhea
 As plasma level approaches 7mEq/L sodium channels become progressively inactivated
which disturbs nerve and muscle function
 It results in
 Impaired cardiac conduction
 Impaired ventricular contraction
 Cardiac arrest
 Convulsions
 Flaccid paralysis
 Respiratory muscle paralysis

DIAGNOSTIC FINDINGS
 Plasma potassium level above5mEq/L
 ECG:-wide flat P wave,prolonged PR intervel, widened QRS, narrow,peakednT wave
 Blood studies may yield false results
 BUN
 Serum creatinine
MEDICAL MANAGEMENT
 In non acute situations dietary restriction of potassium and potassium containing
medication
 In severe hyperkalemia temporary corrective measures include
 Infusion of IV calcium gluconate
 Infusion of insulin and glucose
 Sodium bicarbonate
 Beta agonist albuterol

MEDICAL MANAGEMENT
 Cation exchange resin sodium polystyrene sulfonate
 In hyperkalemia secondary to respiratory acidosis enhance pulmonary function
 In marked renal failure HD or PD
NURSING MANAGEMENT
 Closely monitor the patients at risk for hyperkalemia
 For patients at risk monitor serum potassium levels periodically
 Avoid the chances of false blood results
 Encourage the patient to adhere to prescribed potassium restriction
 Teach the patient about foods which are high and low in potassium
 Pay close attention to solutions concentration and rate of administration
 Caution the patient to use other salt substitutes sparingly if they are taking other
supplementary forms of potassium
 potassium sparing diuretics should not be administered to patients with renal failure
CALCIUM IMBALANCES
 Calcium is an extra cellular and intracellular cation
  Normal plasma range is 4.5-5.5mEq/L or 9-11mg/dl
 99% of calcium is in bones and teeth
 1% is in tissues and intravascular spaces
 About half of the portion in blood is bound to protein
 Remaining half is free(ionized calcium)
FUNCTIONS OF CALCIUM
 Act as catalyst in the transmission and conduction of nerve impulses
 Stimulate the contraction of skeletal, smooth and cardiac muscles
 Maintains normal cellular permeability
 Promotes coagulation of blood
 Promotes absorption and utilization of vitamin B12

HYPOCALCEMIA
 Plasma calcium level below 4.5mEq/L or 8.5mg /dl
 Often reciprocal with phosphurs levels
ETIOLOGY AND RISK FACTORS
 Inadequate intake of calcium
 Inadequate intake of vitamin D
 Deficiency of parathyroid hormone
 Patients with pancreatitis
 Excess amount of sodium
 Alkalosis
 Multiple blood transfusions
 Certain medications

PATHOPHYSIOLOGY
 Decreased calcium causes a decrease in threshold potential
 Smaller stimulus activates action potential
 Increased neuronal excitability and irritability in motor and sensory neurons
 Lack of calcium in the myocardium leads to decreased myocardial contractility
 Decreased calcium absorption in the intestine leads to irritability of intestinal smooth
muscles
 A low calcium level affects blood coagulation
 Bones become more brittle resulting in pathologic fractures
CLINICAL MANIFESTATIONS
 Numbness and tingling of hands, toes and lips
 Emotional liability
 Cardiac insufficiency
 Hypotension
 Dysrhythmias
 Prolonged QT interval
 Carpopedal spasm(trousseau’s sign)
 Facial twitching(chovstek’s sign)
 Prolonged bleeding time
 Seizures
  Laryngeal stridor
 Tetany
 Hemorrhage
 Cardiac collapse
 Eventual death
 Catract
 Dry, sparse hair
 Spontaneous fracture
DIAGNOSTIC FINDINGS
 Plasma calcium level below 4.5mEq/L or 9mg/dl
 Interpret findings in the context of plasma albumin level and pH
 Ionized calcium level below 1.18mEq/L
MEDICAL MANAGEMENT
 Restore calcium balance
 Oral calcium supplements
 Should be given along with milk 30 min before meals
 Diet high in calcium
 If secondary to parathyroid deficiency avoid foods high in phosphate and protein
 IV calcium chloride or gluconate for tetany
 Should be given in 5%dextrose
NURSING MANAGEMENT
 History
 Assess clients cardiac status
 Monitor for bleeding
 Monitor IV sites for infiltration and phlebitis
 Don’t give calcium and bicarbonate in the same IV solution
 Prevent pathologic fractures
 Inform about diet rich in calcium

HYPERCALCEMIA
 Plasma level over 5.5mEq/L or 11mg/dl
 Common electrolyte disorder that can have serious physical complications
ETIOLOGY AND RISK FACTORS
 Metastatic malignancy
 Hyperparathyroidism
 Thiazide diuretic therapy
 Calcium containing antacids
 Prolonged immobilization
 Metabolic acidosis
 Hypophosphatemia

PATHOPHYSIOLOGY
 Destruction of calcium leads to increased calcium release into vascular spaces
 Excessive PTH production promotes calcium retention
 Cell membrane become refractory to depolarization
  This requires a stronger stimulus for response to occur
 Cardiac and smooth muscle activity is impaired
CLINICAL MANIFESTATIONS
 Mild hypercalcemia is usually asymptomatic
 Anorexia,nausea,vomiting
 Polyuria
 Muscle weakness
 Fatigue and lethergy
 Dehydration
 Constipation
 Slowing of bowel transit time
 osmotic diuresis
 Depressed sensorium
 Confusion
 Coma

DIAGNOSTIC FINDINGS
 Plasma calcium level above5.5mEq/L or 11.5mg/dl
 ECG changes:-widened T wave and shortened QT intervel
MEDICAL MANAGEMENT
 Restore calcium balance
 IV normal saline with lasix
 Anti tumor antibiotics
 Calcitonin
 Corticosteroids
 IV phosphate
 Avoid or reduce the dosage of calcium supplements
 Etidronate sodium
 Gallium nitrate
 Restrict high calcium foods

NURSING MANAGEMENT
 Obtain through history
 Assess vital signs
 Bowel sounds, hydration status and renal function should be assessed
 Increase fluid intake
 Teach prevention of complications and safety measures
 If client has confusion, lethargy or coma implement safety precautions
 Assist with resistive range of motion and weight bearing exercise to decrease calcium
loss from bone

PHOPHATE IMBALANCES
 Normal phosphorus level is 1.2-3mEq/L
 1% of phosphorus is contained in vascular spaces
 85% is contained in the bones
  14% is contained in the soft tissues

FUNCTIONS OF PHOSPHORUS
 Promotes strong and durable bones and teeth
 Integral part of energy system and phosphate acid buffer system
 Parathyroid hormone regulates the plasma levels of phosphate
HYPOPHOSPHATEMIA
 Plasma poshosphorus level below 1.2mEq/L

RISK FACTORS
 Periods of increased growth or tissue repair
 Recovery from malnourished states
 Prolonged and excessive intake of antacids
 Administration of high levels of glucose
 Increased sodium
 Lead poisoning
 Metabolic alkalosis
PATHOPHYSIOLOGY
 Affects optimal oxygen and ATP supply

 Impairs conversion of glucose to ATP

 Disruption of mechanism responsible for regeneration of ATP

CLINICAL MANIFESTATIONS
 Decreased cardiac and respiratory function
 Muscle weakness
 Fatigue
 Convulsions
 Brittle bones, bone pain

MANAGEMENT
 Diet and dietary supplementation
 TPN in critically ill patients
 Hyperphosphatemia
 Rare but serious disorder
 Plasma phosphate level below 3mEq/L

ETIOLOGY
 Excessive intake of high phosphate food
 Excess vitamin D
 Hyperparathyroidism
 Addison’s diseases
CLINICAL MANIFESTATIONS
 Tachycardia
 Restlessness
 Palpitations
 Anorexia, nausea, vomiting
 Hyperreflexia
 Tetany
 Dysrhythmias

MANAGEMENT
 Limit high phosphate foods
 Give calcium or aluminum products that promote excretion of phosphate
 Daialysis
MAGNESIUM IMBALANCES
 Second most abundant intracellular cation
 50%magnesium is stored in bone
 49% is in the ICF
 1% is in the plasma
 30% is bound to protein
 15% is combined with anions
 55% in free ionized form
FUNCTIONS
 Transmission and conduction of nerve impulses
 Contraction of skeletal, cardiac and smooth muscles
 Responsible for the transportation of sodium and potassium
 Synthesis and release of PTH
 Necessary for the conversion of ATP to ADP

HYPOMAGNESEMIA
 Plasma magnesium level less than 1.5mEq/L or 1.8mg/dl
 Usually co-exist with other electrolyte imbalances
 Common cause of hypokalemia and hyponatremia
ETIOLOGY AND RISK FACTORS
 Critically ill and alcoholic clients
 Severe or chronic malnutrition
 Malbsorption syndromes
 GI losses
 Renal losses
 Prolonged IV and TPN therapy without magnesium
 Hyperglycemia in DKA
 Alkalosis
 Certain medications

CLINICAL MANIFESTATIONS
 Myocardial irritability
  Anorexia, nausea, abdominal distension
 Depression, confusion, psychosis
 Tetany
 Convulsions
 Vasospasm leading to stroke
 Premature ventricular contractions
 Atrial or ventricular fibrillation
 Prolonged QT intervel, widened QRS complex, broadening of T waves
MANAGEMENT
 Oral magnesium replacement
 IV magnesium
 Monitor vital signs and ECG
 Initiate safety and seizure precautions
 Monitor electrolytes
 Assess deep tendon reflexes
 Avoid giving magnesium in saline solutions
 Teach client and family about foods rich in magnesium
HYPERMAGNESEMIA
 Plasma magnesium level >2.5mEq/L or 3mg/dl
 It can occur with
 Renal insufficiency
 Excessive use of magnesium containing antacids
 Potassium sparing diuretics
 Dehydration from DKA
 Over use of IV magnesium

CLINICAL MANIFESTATIONS
 Dilation of peripheral vessels causing hypotension
 ECG changes include prolonged PR and QT intervel
 Muscle weakness, lethargy, drowsiness
 Loss of deep tendon reflexes
 Respiratory paralysis
 Loss of consciousness
MANAGEMENT
 Saline infusion with a diuretic
 Calcium salts
 Albuterol
 Ventilatory assistance in case of respiratory distress
 Hemodialysis in case of renal failure

NURSING MANAGEMENT
 Monitor high risk clients for early signs of hypemagnesemia
 Assess
 Vital signs
 Respiratory function
 ECG recordings
  Urine output
 Level of sensorium
 Deep tendon reflexes
 Safety and seizure precautions

RESEARCH INPUT
 Therapeutic approach to electrolyte emergencies.
 Schaer M.
 Department of Small Animal Clinical Sciences, College of Veterinary Medicine,
University of Florida,
 Hypokalemia, hyperkalemia, hyponatremia, hypernatremia, hypocalcemia, and
hypercalcemia are commonly seen in emergency medicine. Severe abnormalities in any
of these electrolytes can cause potentially life-threatening consequences to the patient. It
is essential that the clinician understand and correct (if possible) the underlying cause of
each disorder and recognize the importance of the rates of correction, especially with
serum sodium disorders. The recommended doses in this article might have to be
adjusted to the individual patient, and these modifications must be adjusted again to the
pathophysiology of the primary underlying disorder.

CONCLUSIONS
 Electrolyte imbalances are found in all age groups and in all settings
 Nurses play an important role in
 Teaching about positive health behaviors
 Promoting nutritional maintenance
 Assisting in early diagnosis
 Promoting balanced nutrition

Bibliography
 Black M Joyce,”medical surgical nursing- clinical management for continuity of
care”page no:-659-670
 Brunner and suddarth’s”text book of mediacl-surgical nursing” page no:-254-260