NCM 103(LEC): FLUIDS AND ELECTROLYTES

Kidney - produces Urine, Renin, Erythropoietin, Calcitriol

Ureter - transports urine towards the bladder
Urinary Bladder - temporarily stores urine prior to elimination
Urethra – Conducts urine to exterior

Kidney
 Bean Shaped organ located on each side of the vertebra (L12-L3)
 Left kidney larger than right, Right kidney lower than left due to the liver
 To process blood plasma and excrete urine
 Maintains fluid and electrolyte and acid-base balance
 Influence the rate of secretion of antidiuretic hormone and aldosterone
 Synthesizes erythropoietin

Filtration – movement of waster and solute from plasma in the glomerulus,

capsular membrane and into the capsular space of the Bowman’s Capsule
Reabsorption – movement of molecules out of the tubule and into the peri-tubular
blood
Secretions – Movement of molecules out of the peritubular blood and into the
tubular secretion

3 mechanisms to process blood plasma from Urine

 Hydrostatic pressure gradient - Derives the filtration of plasma to
nephrons - Filtrates contains materials that the body needs - Tubular
walls start to reabsorb lose materials back into the blood as filtrate begins
to leave the nephron

Contribution of the different nephrons’ segments to solute and water

homeostasis
 Glomerulus – forms an ultrafiltrate of plasma
 Proximal Tubules
o Reabsorbs isosmotically 65 – 70% of filtrated NaCl and
water
o Reabsorbs 90% of filtrated HCO-3 (by H+ secretions) (early
proximal tubule)
o Ammonia production in nephron
o Reabsorbs almost all filtrated glucose and amino acids
o Reabsorbs K+, Phosphate, Calcium, Magnesium, Urea and Uric
Acid
 o Secrets organic anion (Urate) and cations, Inc. protein-bound
drugs
 Loop of Henle
o Reabsorbs 15-25% of filtrated NaCl
o Countercurrent multiplier as NaCl reabsorbs in excess water
o Active regulation of magnesium secretion
 Distal Tubule
o Reabsorbs a small fraction of filtrated NaCl
o Major site and connecting segment of active regulation of
calcium secretion
 Connecting segment and Cortical collecting tubule
o Principal cells reabsorb Na+ and Cl- and secretes K+ in part
under influence of aldosterone
o Intercalated cells secrete H+, reabsorbs K+ and in metabolic
alkalosis, secretes HCO3-
o Reabsorbs water in presence of antidiuretic hormone
 Medullary collecting tubule
o Site of final modification of Urine
o Reabsorbs NaCl, reduced less than 1meq/L
o Reabsorbs water and urea relative amount of antidiuretic
hormone allowing a dilute or concentrated urine to be present or
excreted
o Secrete H+ and NH3, urine pH can be reducing to 4.5 – 5.0
o Can contribute to potassium balance by reabsorption of K+

Mechanism of Voiding
 Voluntary relaxation of external sphincter muscles of bladder – other
muscles wall contract – forces urine out of the bladder – relaxation of
internal sphincter.
 Voluntary control of micturition is possible if CNS and areas of the brain
are intact and functioning properly

Fluids and Electrolytes

 Water – provides a medium of cellular metabolism
o Transports materials to and from cells
o Acts as solvent
o Regulates body temperature
o Maintains vascular volume
o Aids in digestion of food through hydrolysis
 o Provides mechanism for excretion of water and wastes in the
body
o Maintain physical and chemical constancy of ECF and ICF

 Volume and distribution of water

o Varies with age, sex and amount of adipose tissue
o Accounts 45-80% body weight
o Younger the higher % of body water
o NB – 75%, YA male – 60%, YA Female – 50%

 Water in the body

o Distributed into major compartments
o ICF 2/3 water, ECF 1/3 water
o Distributed to plasma to intravascular fluid compartment to be
the interstitial fluid

 Water Balance
o Exist if water in the form of ingested food
o Sources
 Ingested food and fluids through metabolism
 Metabolic process
 Parenteral and enteral feeding

Fluid volume deficit

 Represents loss of water from the ECF compartment.
 Causes
o Decrease water intake
o Vomiting
o Diarrhea
o Frequent tap water enema
o Systemic infection
o Intestinal obstruction severe burn
 Effects
o Dry skin and mucus secretions
o Cool clammy skin related to peripheral vasoconstriction
o Thirst
o Low urinary output of 100-400cc/24 hours of oliguria
 o Decrease skin turgor
o Acute weight loss
o Week rapid heart rate; flattered neck vein
o Increase in temperature
o Muscles weakness and cramps

 Lab findings
o Dec. CVP, Inc RBC
o Elevated BUN out of proportion creatinine 10:1
o Inc Hct level, RBC suspended in Dec. plasma volume
o K and Na reduced
o Sp. Gravity Inc. (1.025 – 1.035)

Fluid Volume excess

 Caused by increase of water in ECF spaces, generally electrolytes are
retaining as well
 Causes
o Excessive ingestion of NaCl on electrolyte mixture
o Administration of adrenocortical hormones
o Excessive quantities is Isotonic solution of NaCl intravenously
 Effects of ECF excess
o Puffy eyelids
o Shortness of breath and wheezing, Inc. BP and CVP
o Edema, distended neck veins
o Moist crackles
o Acute weight gain
 Labs findings
o Dec. BUN and Hct due to plasma dilution
o In CRF, serum osmolality and NA is decrease due to excessive
water retention
o Urine Na is decrease – kidneys are attempting to excrete excess
volume
o Aldosterone is chronically stimulated (CHF, Nephrotic
syndrome, Cirrhosis) – Urine Na decreased

Shock
  Syndrome in which circulation or perfusion of blood is inadequate to
meet tissue metabolic demands
 Cellular anoxia leads to tissue death unless reversed
 During shock, body struggles to survive, activates of hemostatic
mechanisms to restore blood flow

Classification
1. Hypovolemic shock
a. Refers to which the volume contained within the intravascular
compartment is inadequate for perfusion of body tissue
b. 15 – 25% reduction of intravascular volume
c. Hemorrhagic shock - loss of whole blood about 1/3 of its normal
blood volume
2. Cardiogenic Shock
a. The heart has an impaired pumping ability
3. Septic Shock
a. Caused by infection
4. Neurogenic Shock
a. Caused by alteration in vascular smooth muscle tone
b. CNS injury or complication assoc. w/ medication
5. Anaphylactic Shock
a. Caused by hypersensitivity reaction to pathogens

Stages of Shock
1. Hypovolemic
2. Compensatory
3. Cardiogenic
4. Progressive
5. Irreversible (refractory)
Hypovolemic
 Most common
 Dec. intravascular volume by 15-25%, 750-1300ml blood 70kg person
 Risk factors
o External fluid loss o Internal Fluid shift
 Trauma  Hemorrhage
 Surgery  Burns
 Vomiting  Ascites
 Diarrhea  Peritonitis
 Diuresis  Dehydration
 Diabetes insipidus
 Management
o Goals
 Restore intravascular volume to reverse sequence of
events leading to inadequate tissue perfusion
 Redistribute fluid volume
 Correct the underlying causes of fluid loss
 Interventions
o Treatment of underlying causes
 If hemorrhage, apply pressure to bleeding site
 If diarrhea or vomiting, medication to treat while efforts
are made to identify and treat the cause
o Fluid and blood replacement
o Redistribution
o Pharmacologic therapy
 Nursing Management
o Administer blood and fluids
o Implement other measures
o Oxygen therapy
 o Safe and comfort px

Cardiogenic
 Impaired heart function and supply of oxygen is inadequate for the heart
and tissues
 Types
o Coronary Cardiogenic Shock
 Significant amount of the left Ventricular myocardium
has been damages
o Noncoronary Cardiogenic shock
 Condition that stress the myocardium
 Severe hypoxemia, acidosis, hypoglycemia, tension
pneumothorax)
 Cardiomyopathy, cellular damage, cardia tamponade,
dysrhythmias
 Pathophysiology
o Dec. cardiac contractility
o Dec. SV and CO
o Pulmonary congestion. Des. Systemic tissue perfusion. Dec.
coronary artery perfusion
o Clinical manifestation
 Px. Angina pectoris, dysrhythmias and hemodynamic
instability
 Medical Management
o Correction of underlying cause
 If coronary
 Thrombolytic therapy, angioplasty, CABG,
intra-aortic balloon pump therapy

 In noncoronary
  Replacement of faulty cardiac valve,
correction of dysrhythmia, acidosis and
electrolyte disturbances, treatment of the
tension pneumothorax

o Initial first-line treatment

 Supplemental oxygen
 Controlling chest pain
 Providing selected fluid support
 Administering vasoconstrictive medication
 Controlling HR with medication or pacemaker
 Oxygenation via NC 2-6 lpm
 Pain - IV morphine sulfate
 Laboratory marker monitory (cardiac enzymes)
 Nursing Management
o Preventing cardiogenic shock
 Conserve px energy
 Restore adequate cardiac function and tissue perfusion
o Monitoring hemodynamic status
 Arterial lines
 ECG
 Cardiac, pulmonary and laboratory values
o Administer medication and IV fluids
o Maintain intra-aortic balloon pump counter pulsation
o Enhancing safety and comfort
Circulatory Shock
 Occurs when blood volume is abnormally displaces in the vasculature
(blood pools)
 Caused by either loss of sympathetic tone or by release of biochemical
medication from cells
 Classification
o Septic shock
o Neurogenic shock
o Anaphylactic shock

 Pathophysiology
o Participating events
 Vasodilation
 Active inflammatory response
 Misdistribution of blood volume
 Decreased venous return
 Decrease cardiac output
 Decrease tissue perfusion

 Risk Factors
o Septic shock
 Immunosuppression
 Extremes at age
 Malnourishment
 Chronic illness
 Invasive procedure
 o Neurogenic Shock
 Spinal cord injury
 Spinal anesthesia
 Depressant action of medication
 Glucose deficiency
o Anaphylactic shock
 Penicillin sensitivity
 Transfusion reaction
 Allergic reaction

Septic Shock
 Associated with sepsis, hypotension and hypoperfusion despite adequate
fluid volume replacement
 Medical Management
o Identification of cause
o Remove potential cause
o Fluid replacement due to inflammatory response
o Pharmacologic therapy
o Nutritional therapy
 Nursing Management
o All invasive procedure must be carried out w/ aseptic technique
o Monitor signs of infection
o Administer prescribed IV fluids, medication Inc. antibiotic
agents and vasoactive medication to restore vascular volume
o Laboratory values must be monitored
o Monitor hemodynamic status

Neurogenic Shock
 Result of loss of balance between parasympathetic and sympathetic
stimulation.
 Predominant parasympathetic stimulation that causes vasodilation lasting
for a period of time relative to hypovolemic state
 Vasculature is dilated, blood displaces = hypotensive = Dec systemic
resistance and bradycardia
 Inadequate BP = insufficient perfusion of tissue and cells
  Causes
o Spinal cord injury, spinal anesthesia or CNS damage
o Depressant effect of medication or lack of glucose
 Management
o Restoring sympathetic tone, either through stabilization of spinal
cord injury or position px properly w/ anesthesia
o Administer glucose if needed
 Nursing Managements
o Elevate and maintain the head of the bed at least 30 degrees to
prevent neurogenic shock when receiving spinal or epidural
anesthesia
o Spinal cord injury, immobilize the spine
o Support CV and neurologic function, apply compression socks
and/or elevate legs, prevent pooling of blood in legs (thrombus
formation)
o Administer heparin or LMWH as ordered
o Passive ROM of the immobile extremities helps promote
circulation

Anaphylactic Shock
 Occurs rapidly and life threatening
 Severe allergic reaction when px have already produced antibodies to
foreign substance develop a systemic antigen-antibody reaction
 Medical Managements
o Removal causative antigen
o Epinephrine due to vasoconstrictive effect
o Diphenhydramine (Benadryl) to reverse effects of histamine,
Dec capillary permeability
o Nebulize medication such as albuterol, to reverse histamine-
induced bronchospasm
o CPR if needed
o IV line inserted to provide access for administering fluids and
medication
 Nursing Management
o Assess Patient for allergies or previous reaction to antigens and
communicate the existence of allergies or reaction to others
Electrolytes

Electrolyte Normal Values (mEq/L)

CATION
Sodium (Na+) 135 – 145
Potassium (K+) 3.5 – 5.50
Calcium (Ca+) 8.5 – 10.5
Magnesium (Mg+) 1.5 – 2.5
ANION
Bicarbonate (HCO3-) 24 – 30
Chloride (Cl-) 95 – 105
Phosphate (PO4-) 2.8 -4.5

Na+
 Chief “cation” of ECF
 Takes effect mostly on neuro system
 CNS stimulant; Helps muscle and nerve cells interact
 Influence water distribution in the body (with chloride)

K+
 Chief cation of ICF
 Muscle cardiac contractions
 Cell excitability regulation (heart)
 Nerve impulse conduction
  Control the intracellular osmolality
 High K+ = spastic contractions
 Low K+ = flaccid contractions

Ca+
 Stabilize the cell membrane and reduce its permeability to sodium
 Functions
o Blood – clotting factor IV
o Muscle – contraction of muscle
 Types of muscle
 Skeletal – muscle attached to a bone
 Smooth – GIT
 Cardiac – involuntary muscle
o Bone – Ca+ enhances bone strength
 Ossification - bone formation
 Ostemalaise – weak bone
 Rickets – soft bones (pedia)
o Related disorder
 Spasm
 Tetani
 Trousseau sign – test for Hypocalcemia
o Carpal tunnel spasm produces by inflating a bp of 20mm hg
above the systolic pressure for a few minutes.
 Chvostek sign – gentle tap on the cheek
o Contraction of facial muscle with light tap over the facial nerce
in front of the ear

Mg+
 Muscle relaxant
 Responsible for metabolism of CHON and CHO
 Integrity of Neuro system
 Acts as a catalyst for enzyme reaction
 Modifies nerve impulse transmission and skeletal respone

Po4 –
 Chief anion in ICF
 Essential for energy metabolism
 Maintains acid-base balance
 Combined with calcium = key role in bone and tooth mineralization
 Promotes energy storage of CHON, CHO and fat metabolism
Cl-
 Chief anion in ECF
 Helps maintain osmotic pressure needed by gastric mucosal cell to
produce HCl to breakdown food in absorbable component
 Maintains ECF osmolality

HCO3 – (bicarbonate)
 Kidney – buffer (neutralizer of acid-base)
 Controls acidity of the blood during acid-base imbalance

Sodium
 135-145 mEq/L ECF
 10 mEq/L ICF
 Accounts 90% of ECF
 Abundant solute cation in ECF
 Attracts fluid
 Maintains ECF volume and fluid distribution
 Transits impulse in nerve and muscle fiber
 Maintains acid-base in combination with chloride and HCO
 Min daily requirement – 0,5-2,7g
 Sources
o Canned soups and veggies
o Cheese
o Ketchup
o Processed meats
o Table salts
o Salty snack foods
o Seafoods
 Excreted by kidney, GIT and skin
 Inc Na = Inc fluid in ECF vice versa

Hyponatremia
 <135 – sodium deficiency
 Body fluids diluted
 Water>salt, fluid osmosis
 Cell swells (dec ECF osmolality)
 Severe can lead to (seizure, coma and permanent neuro damage)
 Cerebral edema and hypovolemia
 Types
o Dilutional
 Sodium loss, water gain
o Depletion
 Inadequate sodium intake

 Classification of Hyponatremia
o Hypovolemic
 ECF volume abnormally decreased
 Both sides lose Na and H2O
 Na loss > H2O
 Causes
 Renal
o Osmotic diuresis
o Adrenal insufficiency (Addison’s
Dse)
o Diuretic use (Furosemide or Lasix)
 Non-Renal
o Vomiting
o Diarrhea
o Fistula – abnormal passageway from
the surface of the body to the internal
cavity
o Gastric suctioning
o Cystic fibrosis
o Burns
o Wound dressing
 Hypervolemic
 ECF volume abnormally increased
  Both sides gain (Na and H2O)
 Water and sodium increase in ECF but H2O is
more
 Causes
o HF
o Liver failure
o Excessive administration of
hypotonic IVF
o Hyperaldosteronism

 Euvolemic
 Sodium low due to excessive fluid in body
 No physical signs of fluid excess
 Total body sodium = normal
 Causes
o Glucocorticoid deficiency
 Causing inadequate fluid
filtration by the kidneys
o Hyperthyroidism
o Renal failure
o Syndrome of inappropriate anti
diuretic hormone
 Excessive ADH
 Sign and Symptoms
o Acute initial symptom (115 – 120mEq/L)
 NV
 Anorexia
o Real S/Sx – neurologic
 H/A
 Irritability
 Disorientation
 Muscle twitching
  Tremors
 Weakness
 Changes in LOC
 Short attention span – lethargy/confusion
o If Na+ <110mEq/L
 Neuro status deteriorates further (Cerebral edema)
 Stupor, delirium, psychosis
 Ataxia – poor muscle coordination
 Coma
 Seizure
o Hypovolemia
 Poor skin turgor
 Dry, cracked mucus membranes
 Weak, rapid pulse
 Decreased BP
 Orthostatic hypotension
 CVP decrease, PCWP decrease

 Treatment
o Isotonic fluid replacement
 To restore volume
o High sodium diet
o WOF
 Edema
 HPN
 Wt. gain
 Rapid, bouding pulse
 PAP and CVP increase
 Treatment for severe
o Patient must be in ICU
 Infusion hypertonic saline solution
 3% or 5% saline sol’n in pt is symptomatic
 Monitor for circulatory overload or worsening
neurologic signs
 WOF osmotic demyelination
o Hypertonic – cell shrink – inc. IV
volume overload – brain damage/CE
 May give diuretics
 Administer oral sodium supplement
  Health teaching in diet
 Monitor
 DOB
 Crackles
 Distended JV
 Diagnostics
o Serum osmolality <280mOs/kg
o Serum sodium < 135 mEq/L
o Urine S/G <1.010
o Increase USG and elevated urine sodium > 20mEq/L in pt with
SIADH
o Elevated Hct, plasma chon level
 Memory Jogger HYPERNATREMIA
o S – kin flushed
o A – gitation
o L – ow grade fever
o T – hirst

 Signs and symptoms of Hypernatremia

o Early
 Anorexia
 N/V
 Weakness
 Lethargic
 Confusion
 Stupor
 Seizure
 Coma
 Neuromuscular (twitching, hyperreflexia, ataxia,
tremors)
 Low grade fever
 Flushed skin
 Intense thirst
o Hypervolemia
 Increase BP, CVP, PCWP
 Bounding pulse
 Dyspnea
 Nursing intervention
o Assess neuro status
 o Monitor V/S and record
o Record type of seizure
o Weigh OD
o Accurately monitor I/O
o Monitor sodium and other pertinent test
o Medication and IV therapy

POTASSIUM (K+)
 Major cation ICC/ICF
 Critical role in metabolic cell function
 2% ECF, 98% ICF
 Affects nerve impulses
 Alteration in serum K+ level affects neuromuscular and cardiac
functioning
 Dietary sources
o Dried fruits, nuts, seeds
o Meats
o Vegetables, beans, potatoes, mushrooms, tomatoes, and celery
 Potassium regulation
o Sodium potassium pump – active transport
o Aldosterone – reabsorbs Na+ and excretes K+
o Kidney have no effective mechanism to combat K+ loss and
excretes and decreases K+ level
 K+ intake = 0
 Kidney excrete 10 – 15 mEq/L
 HYPOKALEMIA
o < 3.5 mEq/L
  Moderate 2.5 – 3
 Severe < 2.5
o Narrow level (3.5 – 5.5 mEq/L)
 Slight decrease may cause profound effect
o Causes
 Inadequate intake
 Excessive output
 Prolonged intestinal suctioning
 Recent ileostomy
 Gastric lavage, prolonged vomiting
 Diarrhea, presence of fistula, laxative abuse,
sever diaphoresis
 Renal tubular acidosis
 Cushing syndrome
 Magnesium depletion
 Priods of high stress
 Hepatic disease
 Hyperaldosteronism

o Medication
 Adrenergic – epinephrine, non epinephrine
 Antibiotics
 Amphotecin B
 Carbenicillin
 Gentamicin
 Cisplatin
 Corticosteroids
 Diuretic – loop diuretics – Lasix
 Insulin
 Laxatives
o Mnemonics
 S – skeletal system weakness
 U – wave
 Flattened inverted T wave, depressed ST
segment and U wave appearance
 C – constipation
 T – toxic effect of digoxin
 I – irregular, weak pulse
  O – orthostatic hypotension
 N – numbness (w/ cramps)
o Treatment
 High K+ diet
 K+ supplements
 Oral or IV or both
 Once balanced
 K+ sparing diuretics
o Aldosterone
o Nursing Consideration
 Monitor V/S
 Hypokalemia commonly Assoc, w/
hypovolemia
 Check HR rhythm and ECG
 Assess RR depth, rate, and pattern
o Hypokalemia weakens or paralyzes
respiratory muscles
 Monitor K+ level
 Monitor and document I/O
 Insert and maintain IV access
 WOF IV infusion site for infiltration
 Oral K+ supplement with food
 Do not crush slow release tablets
 Proved safe environment
 Check for constipation
 Abdominal distention and decrease in BS
 Do not use laxative that promotes K+ loss
 Do not take digoxin with K+
 Toxicity S/s: HR irregularities, anorexia, N/V
o HYPERKALEMIA
 > 5.50 mEq/L
 Moderate = 6.1 -7.0
 Severe = > 7.0
 Causes are less than hypokalemia but more profound serious
 Hydrogen ion pushes K+ outside cell
 Cell injury causes the releases K+ into ECC
 Causes
 Excessive intake
 Upsetting balance
  Little output
o Acute and chronic renal output
o Dialysis
o Diabetes
o SCD
o SLE – chronic inflammatory disease
o Addison’s disease
o hyperaldosteronism
 Injury moves it out
 Kayexalate – sodium polystyrene sulfonate
 Sorbitol or another osmotic substance should be
given with kayexalate to promote excretion of
excess K+
o Action time: 4-6 hours
o Intestines – Na moves across – bowel wall
– into blood – ATPase pump – K moves
out of blood – loose stools remove K

Calcium
 Bones and teeth
 Inverse relationship with PO4
 Functions
o Formation and mineralization of bones
o Muscular contractions and relaxation
o Cardiac function
o Blood coagulation
o Promotes absorption and utilization of vit B12
o Activates exocytosis of neurotransmitters and other cellular
secretions
o Activates cellular enzymes
 Calcitonin – secreted by C cells in thyroid gland
 Calcitriol – derived from Vit. D
o Enhances intestinal absorption
 Calcium imbalances
o Hypocalcemia (<4.5 mEq/L)
 o Hypercalcemia (> 5.8 mEq/L)
 Regulation
o GIT – absorbs Ca in the intestines with the help of vit D
o Kidney - Ca is filtered in the glomerulus and reabsorbed in the
tubules
o PTH – increases Ca by bone reabsorption, increase intestinal
and renal Ca reabsorption and activation of vit D
o Calcitonin – reduces bone reabsorption, inc. Ca and
Phosphorous deposition in bones and secretion in urine
 HYPERCALCEMIA
o Etiology
 Overuse of calcium supplements and antacids
 Excessive vit A and D
 Malignancy
 Hyperthyroidism
 Thiazide diuretic
o S/Sx
 Anorexia
 N/V
 Polyuria
 Muscle weakness
 Fatigue
 Lethargy

o Dx
 Increase serum Ca
 ECG
 Shortened QT interval, ST segments
 Inc. PTH levels
 X rays – osteoporosis
o Management
 IV – 0.9NaCl
 IV – Phosphate
 Diuretics – Furosemide
 IM calcitonin
 Corticosteroids
 Dietary restriction
o Nursing Management
 Assess VS. apical pulse and ECG, Bowel sounds, renal
function and hydration status
  Safety precautions in unconscious px
 Inc. fluid intake
 Monitor cardiac rate and rhythm
 HYPOCALCEMIA
o Etiology
 Removal of parathyroid gland
 Vit D and Mg deficiency
 Furosemide
 Infusion of citrated blood
 Inflammation of pancreas
 Renal failure
 Thyroid CA
 Low albumin
 Alkalosis
 Alcohol abuse
 Osteoporosis
o S/Sx
 Tetany
 Chvostek
 Trousseau’s
 Seizures
 Depression
 Impaired memory
 Confusion, delirium, hallucination
 Hypotension
 Dysrhythmias
o Dx
 Dec Ca level
 ECG: prolonged QT interval
o Management
 Calcium salts
 Vit D
 Diet
o Nursing management
 Monitor cardia status, bleeding
 Monitor IV sites for phlebitis
 Seizure precautions
 Reduce smoking

Magnesium
 Second to K+ in ICF
 Functions
o Intracellular production and utilization of ATP
o Protein and DNA synthesis
o Neuromuscular irritability
o Produce vasodilation of peripheral arteries
 HYPERMAGNESEMIA
o M > 2.1 mEq/L
o Etiology
 Use of Mg antacid,
 K sparing diuretics
 Renal failure
 Mg medication, DKA
 Adrenocortical insufficiency
o S/Sx
 Hypotension
 N/V
 Flushing
 Lethargy
 Difficulty speaking
 Dec LOC
 Coma
 muscle weakness
 Paralysis
 Depressed tendon reflexes
 Oliguria
 Dec. RR
o Management
 Discontinue Mg supplements
 Loop diuretics
 IV Ca gluconate
 Hemodialysis
 Hemodialysis
o Nursing Management
 Monitor VS
 DTR and changes LOC
 Seizure precautions
 HYPOMAGNESEMIA
o Mg < 1.5 mEq/L
o Etiology
  Alcohol withdrawal
 Tube feeding
 Diarrhea
 Fistula
 GIT suctioning
 Drugs (antacids, aminoglycoside, insulin therapy)
 Sepsis
 Burns
 Hypothermia
o S/Sx
 Hyperexcitability w/muscle weakness
 Tremors
 Tetany
 Seizures
 Stridor
 Chvostek and trousseau’s sign
 ECG change
 Mood change
o Dx
 Serum Mg level
 ECG
 Prolong PR and QT interval
 ST depression
 Widened QRS
 Flat T wave
 Low albumin

o Management
 Diet
 IV Mg sulfate via infusion pump
o Nursing management
 Seizure precautions
 Test ability to swallow, DTR
 Monitor I/O, VS during Mg admin,

Chloride
 Major anion in ECF
 Inc. Na reabsorption causes inc. Cl reabsorption
 Functions
o Major component of gastric juices aside from H+
 o Together with Na regulates plasma osmolality
o Participates in Cl shift – inverse relation with bicarbonate
o Acts as chemical buffer
 Regulation
o Indirectly regulated as an effect of Na homeostasis.
o Sodium is retained or excreted, Cl passively follows
 Chloride imbalance
o Hyperchloremia (> 105 mEq/L)
o Hypochloremia (< 95 mEq/L)
 HYPERCHLOREMIA
o Etiology
 Sodium excess
 Loss of bicarbonate ions
o S/Sx
 Tachypnea
 Weakness
 Lethargy
 Deep, rapid respirations
 Diminished cognitive ability and hypertension
 Dysrhythmias
 Coma
o Dx
 Inc. serum Cl
 Dec serum bicarbonate
o Management
 Lactated ringers solution
 IV Na bicarbonate
 Diuretics
o Nursing management
 Monitor VS, ABG, I/O
 Neurologic, cardiac, respiratory changes
 HYPOCHLOREMIA
o Etiology
 CL deficient formula
 Salt restricted diet
 Severe vomiting and diarrhea
o S/Sx
 Hyperexcitability of muscles
 Tetany
 Hyperactive DTR
  Weakness, twitching muscle, cramps
 Dysrhythmias, seizure
 Coma
o D/Sx
 Dec serum Cl level
 ABG’s metabolic alkalosis
o Management
 Normal saline/half strength saline
 Diet, avoid free bottled water
o Nursing management
 Monitor I/O, ABG, VS, LOC
 Muscle strength and movement

Phosphate
 Major anion in ICF
 Reciprocal relationship with Ca
 PTH – inc. bone reabsorption, inc. PO4 absorption from GIT, inhibit
PO$ excretion from kidney
 Calcitonin – inc. renal excretion of PO4
 Function
o Component of bones
o Needed to generate ATP
o Component of DNA and RNA and phospholipids
 Regulation
o PTH – inc renal excretion of phosphate – dec plasma phosphate
o No renal phosphate imbalance

 HYPERPHOSPHATEMIA
o PO4 > 4.5
o Etiology
 Excess vit D
 Renal failure
 Tissue trauma
 Chemotherapy
 PO4 medication
 Hyperparathyroidism
o S/Sx
 Tetany
  Tachycardia
 Palpitation
 Anorexia
 Vomiting
 Muscle weakness
 Hyperreflexia
 Tachycardia
 Soft tissue calcification
o Dx
 Inc. serum phosphorous level
 Dec. Ca level
 X ray- skeletal changes
o Management
 Limit dairy
 Dialysis
o Nursing management
 Dietary restrictions
 Monitor signs of impending hypocalcemia and changes
in urine output

 HYPOPHOSPHATEMIA
o PO4 < 2.5 mg/dl
o Etiology
 Administration of calories in severe CHON – caloric
malnutrition (iatrogenic)
 Chronic alcoholism
 Prolonged hyperventilation
 Poor dietary intake
 DKA
 Thermal burns,
  Respiratory alkalosis
 Antacid which bind w/ PO4
 Vit D deficiency
o S/sx
 Irritability
 Fatigue
 Apprehension
 Weakness
 Hyperglycemia
 Numbness
 Paresthesia
 Confusion
 Seizure coma
o Dx
 Dec serum PO4 level
o Management
 Oral or IV phosphorous correction
 Diet
o Nursing management
 Introduce TPN solution gradually
 Prevent infection