A.

Fluid and electrolyte balance

1. Body fluids
a. Function of body fluids
b. Body fluid compartments
2. Electrolytes
a. Breakages
b. Functions of electrolytes
3. Movement of water & electrolyte
a. Passive transport
aa. Diffusion
bb. Osmosis
cc. Filtration
b. Active transport
4. Concentration of fluids+
a. Isotonic
b. Hypotonic
c. Hypertonic
5. Mechanisms in regulating F & E Balance

B. Types of Fluid balance / Imbalance

1. Saline balance / imbalance

a. Saline deficit
b. Saline excess
2. Water balance / imbalance
a. Water deficit
b. Water excess
3. Edema

C. Electrolyte Balance / Imbalance

1. Potassium Balance / Imbalance

a. Hypokalemia
b. Hyperkalemia
2. Calcium Balance / Imbalance
a. Hypocalcemia
b. Hypercalcemia
3. Phosphate Balance / Imbalance
a. Hypophosphatemia
b. Hyperphosphatemia
4. Magnesium Balance / Imbalance
a. Hypomagnesemia
b. Hypermagnesemia

22
 D. Acid –Base Balance / Imbalances

1. Physiological Mechanisms in Regulating acid-base balance

2. Acidosis
a. Respiratory b. Metabolic
3. Alkalosis
a. Respiratory b. Metabolic

BODY FLUIDS

- Refers to body water in which electrolytes are dissolved.

- Been described as “a sea within”
- Water is the largest single constituent of the body, representing 45% - 75% of the body
weight, depending on age, gender & body fat.
- In the newborn infant, almost ¾ of the body weight is water, with the greatest percentage
found in extracellular compartment.
- By adulthood, the young male’s body water is only 60% and 2/3 of this is in the
intracellular compartment.
- In the average young female, only approximately 50% of body weight is water. Reason?
Increased amount of fat in women which is essentially water-free.

Functions of Body Fluids

1) Transport nutrients to the cells and carries waste products away from the cells.
2) Maintains blood volume.
3) Regulates body temperature.
4) Serves as aqueous medium for cellular metabolism.
5) Assists in digestion of food through hydrolysis.
6) Acts as solvents in which solutes are available for cell function.
7) Serves as medium for the excretion of waste products.

Compartments of Body Fluid:

a) Intracellular (ICF) – within the cell, approx. 2/3 of the body fluid, located primarily in
the skeletal muscle mass, provides the aqueous medium for cellular chemical function.
b) Extracellular (ECF) – outside the cell, maintains blood vol. & serves as the transport
system to & from the cells.
1) Interstitial fluid – fluid between the cells, fills spaces between most cells and
comprises 15% of body weight, lymph is an example
2) Intravascular fluid – fluid in the blood vessels, the PLASMA, is the watery
colourless fluid of lymph and blood in which erythrocytes, leucocytes and
platelets, are suspended and comprises 5% of body weight, approx. 3L of the ave.
6L of blood vol. is made of plasma. The remaining 3L is made up of other blood
components.
3) Transcellular – 1- 3% of body weight, the smallest division of the ECF
compartment and contains approx. 1-2L of fluid in any given time, examples are

23
 CSF, pericardial, synovial, intraocular, pleural fluids, sweat, and digestive
secretions.

ELECTROLYTES

- chemical compounds in solution that have the ability to conduct an electrical current.
- They break into ions:
a) cations – positively charged (Na, K, Ca, Mg, Hydrogen ions)
b) anions – negatively charged (Cl, Bicarbonate, phosphate, sulfate, proteinate ions)
- they are distributed in different concentrations in the intracellular, intravascular &
interstitial.

General Functions of electrolytes:

a) promote neuromuscular irritability

b) maintain body fluid volume and osmolality.
c) distribute body water between compartments
d) regulate acid-base balance

Movements of Water and Electrolytes

1. Passive transport

A. Diffusion – movement of particles from an area of higher to lower concentration within one
compartment.
B. Osmosis – movement of fluid from an area of lower concentration to higher concentration
across the semi-permeable membrane.
 Osmotic pressure – is the drawing power for water – a high concentration of particles has a
high osmotic pressure and draws water.
 Osmolality - reflects the concentration of fluid that affects the movement of water between
fluid compartments by osmosis. Also measures the ability of a solution to create osmotic
pressure and affect movement of water. (mOsm/kg)
 Osmolarity - reflects the concentration of solutions. (mOsm/L)

C. Filtration - is the process by which water and diffusible substances move together in
response to fluid pressure. This process is active in capillary beds.

2. Active transport – movement of ions from an area of lesser to greater concentration with an ion
pump. (Na –K pump)

Concentration of Fluids

A. Isotonic – Exerts the same osmotic pressure as that found in plasma.

Osmolarity is 240-340mOsm/L.
B. Hypotonic – Exerts less osmotic pressure than that of blood plasma. Osmolarity is less than
240 mOsm/L
C . Hypertonic - Exerts a higher osmotic pressure than that of blood plasma. Osmolarity is more
than 340mOsm/L.

24
Mechanisms in Regulating Fluid & Electrolyte Balance

A. Renal system –kidney (filtration in the glomerulus)

B. CNS – hypothalamus (thirst center)
C. Endocrine system – pituitary (secretes ADH)

Types of Fluid Balance & Imbalance

A. Saline – ECF, reflects the volume of water and salt

B. Water – osmolar proportion of water and salt (concentration)

SALINE BALANCE

 refers to maintaining the proper volume of ECF and the three mechanisms involved in
regulating saline balance

Aldosterone
 a major regulator of saline balance (ECF volume)

SALINE IMBALANCE

 changes in the volume of extracellular fluid compartment.

Mechanisms in Regulating Saline balance (ECF Volume)

A. Pituitary Gland
Ineffective blood volume (decrease blood circulation / decrease ECF volume)  stimulates
adrenal cortex  to secrete aldosterone  distal tubules  collecting ducts  increase Na
reabsorption  increase saline retention  thus increases in volume of water & Cl thereby
relieving saline imbalance.

B. Atrial Natriuretic
Atrial distention (increase ECF)  release peptides  acts on the kidney  increase renal
excretion of Na & water to relieve distention.

C. Neural mechanism
Decrease ECF volume  stimulate renal sympathetic nerves  release of renin  stimulates
kidney  dec. renal secretion of saline  increase ECF volume  atrial distention 
mechano –receptors in the wall of L atrium  dec. activity of sympathetic nerve  increase
excretion of saline by kidney.

SALINE DEFICIT

 ECF volume deficit

 Isotonic contraction
 Isosmotic dehydration

25
  Hypovolemia
 Extracellular volume depletion

Causes:

1. vomiting
2. diarrhea
3. extreme diaphoresis
4. blood loss through hemorrhage
5. burns
6. bed rest
7. fistula drainage
8. salt wasting disorder
9. third space fluid accumulation

Third-space fluid shift - or “third spacing” where there is a loss of ECF into a space that does not
contribute to the equilibrium bet. ICF & ECF.
“Third spacing” occurs in:
a) ascites
b) burns
c) peritonitis
d) bowel obstruction
e) massive bleeding into a joint or body cavity.

10. NGT suctioning

11. excessive use of diuretics
12. intestinal decompression

Clinical Manifestations

1. Weight Loss (except with third space accumulation)

2. Postural BP Drop
 to elicit this sign, BP and pulse are measured 2x; first, while a person is lying supine &
second while the person is standing erect or sitting with legs dependent
 if blood volume is normal, there will be little change in systolic pressure and a slight rise (5-
10 mmHg) in diastolic pressure
 if blood volume is diminished, the systolic BP will decrease more than 15mmHg, the diastolic
pressure will decrease to 10mmHg or more, and the pulse will increase when the upright
position is assumed.
 Postural BP drop ay indicate saline deficit of 2 liters or more

3. Increased small vein filling time

 a small vein in the hand or foot is occluded with a finger
 the extremity must be below the level of the heart. While the vein is occluded, it is milked
toward the heart so that it is flat.
 The time for the vein to fill is noted when the finger is released. If the cardiovascular system
is not impaired, a small vein filling time greater than 3-5 seconds denotes a saline deficit.

26
 4. Neck veins flat or collapsing with inspiration
5. Dizziness, syncope
6. Oliguria
7. Decreased CVP
 done by means of a catheter introduced through the median-cubital vein to the sup. vena cava.
8. Decreased skin turgor
 assessed by pinching up the skin over an area like the sternum, then releasing it to see how
quickly it returns to its normal position.

9. Longitudinal furrows in the tongue

 develops after a loss of 3 or more liters of saline.
10. Dryness of opposing mucous membrane (gums)
11. Hard, dry stools
12. Decreased tears and sweat caused by prolonged severe saline deficit
13. Sunken eyeballs
14. Oliguria / anuria
15. Hypovolemic shock extreme saline deficit

Laboratory Values in Saline Deficit

a. Urinalysis – increase Cl
b. Blood studies - increase BUN, increase hct, increase plasma proteins, increase Na

Nursing Diagnosis & Interventions

1. Dx – Fluid volume deficit

a. Weigh the patient daily
b. I & O monitoring
c. BP (postural) changes
d. Measure circulating blood volume
2. Dx – Potential for injury related to postural hypotension
a. Rise slowly
b. Exercise
3. Dx – Activity intolerance
4. Dx – Knowledge deficit regarding home management of emesis & diarrhea.
a. Teaching the patient to replace body fluid losses with both salt and water to prevent saline
deficit. (give bouillon)

Medical Therapy and Collaborative Interventions for Patients

1. Saline replacement thru IV related to complication of medical therapy.

2. Dx – Potential for injury related to complication

SALINE EXCESS

 ECF volume excess

 Isotonic expansion

27
  Hypervolemia
 Circulatory overload

Causes of Saline Excess

1. Endocrine imbalance, which includes:

a. hyperaldosteronism – musc. Weakness, polyuria, polydipsia, hpn
b. Cushings’s syndrome – more in females, adiposity of neck, face, trunk, kyphosis, hpn, muscle
weakness / males – impotence
c. Glucocorticoid therapy
2. Secondary to disease process
a. chronic renal failure
b. congestive heart failure
c. cirrhosis
3. Excess intravenous infusion of saline solutions ( 0.9% Saline, Ringer’s)

Clinical Manifestations

1. Weight gain (0.5 kg/day) - sign of volume expansion

2. Edema
3. Vascular expansion
4. Crackles (lungs in form of rales)
 because of fluid accumulation in the lung
5. Dyspnea, orthopnea (circulatory overload)
6. Increase CVP (5-10 cm H2O) – R atrium

Laboratory Values in Saline Excess

1. CVP elevated
2. CXR – accumulation of fluids in the lungs
3. Blood studies – serum Na normal
4. Hematocrit (normal or decrease)
 depending on the cause if occur slowly, hct remains normal

Nursing Diagnoses & Interventions

1. Fluid Volume Excess

a. Continuous monitoring of I & O (fluid)
b. Assessment of lungs (crackles)
c. Daily weighing (edema)

2. Impaired gas exchange

 diagnosis for patients with saline excess in whom fluid has accumulated in the lungs
a. Put patient in semi-Fowler’s position
 fluid will shift on lower part of the lungs thus providing space for air.
1. Na-restricted diet
2. Diuretics
3. Treatment of the underlying caus

28
Collaborative
1. Teaching patients about home management of diet and meds.

WATER BALANCE AND IMBALANCE

Water balance
 refers to the maintenance of the proportion of salt to water in the blood.

Important facts:
1. Serum Na concentration is a useful measure of water balance. The normal range of serum Na
is 135 – 145 mEq/L in adults of all ages.
2. If the serum Na is decreased –
 the osmolality of blood is decreased
 blood is less concentrated than normal
 blood has excess water relative to the amount of salt.
3. If the serum Na is increased –
 osmolality of blood has increased
 blood is more concentrated
 the blood has a deficit of water relative to the amount of salt

Normal & Abnormal Routes of Water Entry and Exit

Route of Entry Average Volume (per 24 hours)

Gastrointestinal
Oral
Drink 1200 ml
Water in food 1100 ml
Metabolic water 300 ml
Rectal ---
Parenteral ---

Route of Exit
Renal 1500 ml
Respiratory 400 ml
Gastrointestinal
Fecal 100 ml
Emesis ---
Fistula Drainage ---
Skin
Insensible perspiration 600 ml
Drainage from lesions ---
Other
Paracentesis procedures ---
Hemorrhage ---______________
Total : 2600 ml average/ 24 hr

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The major regulators of oral water intake are:
1. Thirst
2. Habit patterns
3. Social influence

Three major mechanisms of thirst

A. Cellular dehydration thirst

 occur when an increase in the osmolality of ECF causes intracellular dehydration of
osmosensitive cells in the lateral preoptic area of the brain.

Cycle:
increase in osmolality of ECF

intracellular dehydration of osmosensitive cells in the lateral preoptic area of the brain

thirst

B. Baroreceptor – mediated thirst

 occurs when decrerased venous return stimulates low pressure baroreceptors in the R atrium

Cycle:
decreased venous return

baroreceptors in the R atrium

neural stimuli

CNS (traveled via vagus nerve)

Thirst

C. Angiotensin – mediated thirst

 occurs when a decrease in effective circulating blood volume triggers the renin – angiotensin
system
 Angiotensin II & III circulate in the bloodstream and pass through fenestrated capillaries into
areas near the 3rd ventricle of the brain.
 Also occurs with hemorrhage.

Cycle of Urine Excretion

Increase in osmolality of blood  hypothalamus  pituitary gland  release of ADH

 collecting ducts of kidney  reabsorption of water back to the blood stream 
dilute blood  restoring osmolality

Note: The excretion of urine (of water) is controlled by anti-diuretic hormone (ADH)

30
 TYPES OF WATER IMBALANCE

Water Deficit
 hypernatremia
 water depletion
 hypertonicity
 hyperosmolar imbalance ( osmolality)

Causes:
I - Loss of water relative to salt
1. Renal
a. diabetes insipidus (salt is gain because of polyuria)
b. osmotic diuresis (polyuria)
c. renal concentrating disorder
d. renal failure
2. Other sources
a. prolonged diarrhea w/o water replacement
b. excessive sweating w/o water replacement
c. dysfunctional humidifier of mechanical ventilator (there is inhalation of dry air so there is
reinhalation of air and serum Na is retained)

II – Gain of salt relative to water

( I salt because of poor water intake)
1. Decrease water intake
a. No access to water
b. Prolonged nausea
c. Difficulty swallowing fluid (Parkinson’s disease)
d. Inability to response to thirst
2. Increase salt intake
a. By means of tube feeding
b. Half and half for ulcer diet
c. Excess hypertonic NaCl or NaHCO3
d. Near drowning in salt water

Clinical Manifestation of Water Deficit

Pathophysiology
  H2O   osmolality  osmosis  ICF  ECF  attempt to restore osmolality 
cell shrivels  cell dysfunction

1. Serum Na is above normal (blood is concentrated) – 135 – 145 mEq/L

2. Thirst (due to lack of water)
3. Oliguria
4. Confusion
5. Lethargy
6. Mild muscle weakness
7. Seizures
8. Coma (varies in severity)

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Laboratory Values in Water Deficit
1. Urinalysis -  in specific gravity of urine more than 1.030
Normal urine specific gravity is 1.010 – 1.030
2. Blood studies -  in serum Na ,  serum protein,  hct

Nursing Dx / Interventions
1. Potential for injury related to decrease level of consciousness
Interventions:
a. Institute safety measures such as raising of siderails
b. Turning from side to side (preventing pneumonia or bed sores)
c. Covering the eye with wet pads
2. Self – care deficit
a. Ongoing assessment of LOC

Medical Therapy
1. Replacement of fluid loss by IVF or oral route
a. institute or encourage oral fluid intake
b. administer in small amount
c. help patient in taking his I & O measurement. Give him a responsibility in his own care.

Nursing Mx
1. Administration of fluid such as IVF
2. Proper regulation and infusion of fluid
 if pt. has cerebral edema, do not increase abruptly.

Nursing Dx of Cerebral Edema

1. Potential for injury related to complications of medical therapy
Complications:
1. cerebral edema (therapy too rapid)
2. rebound fluid excess (therapy excessive)
3. infection
4. infiltration because of IV therapy

Water Excess

 hyponatremia ( serum Na -  135 mEq/L)

 water intoxication
 hypotonicty

Causes:

I – General Etiology : Gain of Water Relative to Salt

A. Endocrine
1. Stimulation of ADH
a. stressors
b. postsurgical state
c. nausea
d. pain

32
 2. Ectopic production of ADH

B. Iatrogenic – caused by medical therapy

1. excessive tap water enema
2. excessive infusion of D5W
3. excessive use of ultrasonic nebulizer
4. hypotonic irrigating solution (by process of osmosis)
5. excessive water ingestion after poisoning
6. excessive water ingestion before an UTZ ezamination

C. Others
1. Psychogenic polydipsia – excessive thirst
2. Excessive beer drinking
3. Near drowning in fresh water
4. Overdose of barbiturates

II - General Etiology: Lost of Salt Related to Water

A. Renal
1. salt wasting renal disease
2. use of many types of diuretics (thiazides)

B. G.I. – due to water replacement not by salt

1. nasogastric suction
2. vomiting
3. diarrhea
4. hypotonic irrigation solutions

C. Other
1. burns
2. excessive sweating

Clinical Manifestations of Water Excess

Pathophysiology:
  H2O   osmolality  osmosis  ECF  ICF  attempt to restore osmolality 
cell swollen  cell dysfunction

Clinical Manifestations
1.  serum Na
2. malaise
3. headache
4. confusion
5. lethargy
6. seizures
7. coma

Nursing Intervention & Dx

 same as in water deficit

33
Medical Therapy
1. Restrict H2O intake below the daily insensible losses (1000 ml)
 the kidney will excrete the excess water.

Nursing Dx and Ix
1. Alteration in Comfort: Thirst
a. wetting of lips
b. plan the timing of fluid intake over 24hrs with the person involved.
c. have the indiv. Choose their own favorite fluids
d. suggest eating meals dry with fluids allowed between meals
e. provide very cold, rather than lukewarm or hot liquids
f. use an insulated glass to provide the illusion of volume
g. clarify fluid restriction with the dietary dept. to prevent confusion
h. have indiv. maintain their own intake and output records
i. suggest moistening of oral membranes with liquid before swallowing
j. teach sham drinking

2. Potential for injury related to complications of medical therapy

a. careful nursing surveillance for the following potential problems:
1. neurological damage (therapy too rapid)
2. rebound hypernatremia (therapy excessive)
3. saline excess
4. infections / infiltrations

Management
1. administration of diuretic (furosemide)
2. administration of ADH blocking agent in the form of demeclocycline or LiCO3.

EDEMA

 fluid accumulation of the interstitial space

 may be a sign of saline excess
 governed by the net result of 4 several forces:

1. Blood hydrostatic pressure

 pressure of blood against the capillary walls in an outward direction.

2. Interstitial fluid hydrostatic pressure

 pressure of interstitial fluid against the capillary walls in an inward direction

3. Blood colloid osmotic & oncotic pressure

 tends to pull fluid inward into the capillaries

4. Interstitial fluid osmotic pressure

 tends to pull fluid outward from the capillaries

Capillary Mechanisms for Edema Formation

1.  Blood Hydrostatic Pressure

34
 a.  capillary flow
1. local infection
2. inflammation
b. Venous congestion
1. external pressure
2. venous thrombosis
3. right heart failure

2.  blood osmotic pressure

a.  serum albumin
1. loss of albumin
2. nephrotic syndrome
3. protein-losing enteropathies
4. liver diseases (cirrhosis)

3.  interstitial fluid osmotic pressure

a.  capillary permeability
1. burns
2. inflammation
3. hypersensitivity reactions
4. toxins
5. trauma

4. Impaired lymphatic drainage

a. obstruction of the lymph node by a tumor
b. surgical removal of lymph nodes
c. obstruction of lymph nodes by parasites

Nursing Assessment of Edema

1. Patient should be weighted at the same time each day.
2. Careful I & O monitoring.
3. Measurement of the girth of parts.
4. Checking for edema in dependent body parts.
5. Alert in the presence of periorbital edema (@ eyes)
6. Question patients about shoes or rings that become too tight.

Pitting Edema
 pressing gently of a part by a finger when indentation is present.

Nursing Dx & Ix
1. Potential for impairment of tissue integrity related to edema
 edematous tissues are susceptible to injury such as pressure sores or sheet burns
a. Careful skin care.
b. Positioning (elevation)
 elevation is C/I in persons with arterial disease.
c. Keeping the patient’s fingernails short or at least smoothly manicured.

35
 2. Alteration in comfort and disturbance in body image
a. Elevation of extremity / part to promote venous return.
b. Administering / doing ROM’s for edema with muscle paralysis

Medical Therapy and Collaborative Interventions

1. Use of elastic stockings to enhance venous return.
2. Administration of diuretics or a Na-restricted diet.

ELECTROLYTE BALANCE AND IMBALANCES

Electrolytes
 salts, found in every body fluids
 K, Ca, PO3, Mg (major electrolytes)
 enter the body primarily in the diet then they enter the ECF and distributed to some other
body electrolyte pool (bones / inside cells)

Normal Routes of Exit

1. urine
2. feces
3. sweat

Abnormal Routes
1. fistula drainage
2. emesis
3. gastric or intestinal suction
4. paracentesis
5. exudates

K BALANCE & IMBALANCES

Normal range – 3.5 – 5.0 mEq/L

Kalium – Latin word for K.

Potassium Homeostasis
1. enters cells through an active transport mechanism
2. both insulin and epinephrine cause K to enter cells
3. exercise causes K to exit cells initially
4. pH of ECF also affect the distribution

Factors that causes K shift

A. Accumulation of carbonic acid
 may cause a mild ECF shift
B. Accumulation of mineral acids
 causes significant extracellular K shift
C. Accumulation of organic acids
 does not in itself cause a K shift.

36
HYPOKALEMIA
 serum K concentration drops below 3.5 mEq/L

Causes:
1.  K intake
a. Non-iatrogenic
1. anorexia
2. fad diets
3. fasting
b. iatrogenic
1. NPO orders
2. prolonged IV therapy w/o K

2. Entry of K into cells

3. Increased K excretion
4. K loss by abnormal route

Clinical Manifestations in K
1. serum K below normal
2. postural hypotension
3. abdominal distention
4. diminished bowel sounds manifestations of the unresponsiveness
5. constipation of smooth muscle of GI tract
6. skeletal muscle weakness
7. flaccid paralysis
8. polyuria, nocturia
9. cardiac arrhytmias
10. ECG changes : ST depression, inverted T waves, U waves, QT prolongation

Note:  K is manifested in dysfunction of all 3 kinds of muscle:

a. smooth
b. skeletal
c. cardiac

Nursing Dx & Ix
1. Alteration in bowel elimination related to constipation.
a. Routine assessment of bowel sounds
2. Potential for injury related to postural hypotension
a. Remind to rise from bed or chair slowly to prevent fall.
3. Potential for injury related to muscle weakness
4. Impaired physical mobility related to muscle weakness.
5. Self-care deficit related to severe muscle weakness or flaccid paralysis.
a. Formulate safety measures.
b. Ongoing assessment of the ability to function
c. Assistance with activities in daily living
d. Frequent turning and ROM exercises to avoid complications of immobility until function
is restored.
6. Potential for ineffective breathing pattern related to respiratory muscle weakness.

37
 a. Assess respiratory function frequently.
b. Position to facilitate respiration (Semi-fowler’s)
7. Knowledge deficit related to or noncompliance with prescribed K therapy
a. Patients must be taught how to incorporate high K foods into their diet

Medical Therapy for  K

1. Oral or IV K replacement

Collaborative Ix for patients with Hypokalemia

8. Potential for injury related to complications of oral replacement
Pt. must be monitored:
1. GI irritation or ulceration
2. Rebound hyperkalemia (if oliguria develops)

9. Potential for injury related to complications of IV K replacement

Potential problems:
1. cardiac arrhytmias (therapy too rapid)
2. rebound hyperkalemia (therapy excessive)
3. inflammation, infection, infiltration (out of vein)

HYPERKALEMIA
 serum K concentration above 5.0 mEq/L
 excess of K in the ECF

Causes of Hyperkalemia:
1. Increased K intake
2. Movement of K out of cells
3. Decreased K excretion

Clinical Manifestations
1. serum K above normal
2. intestinal cramping
3. diarrhea
4. skeletal muscle weakness
5. flaccid paralysis
6. cardiac arrhythmias
7. cardiac arrest
8. ECG changes: peaked narrow T waves, shortened QT intervals, widened QRS, sine wave

Lab. Values
1. acidosis
Nursing Dx & Ix
1. Alteration in bowel elimination related to diarrhea
a. replenishment of F & E.
b. careful skin care to prevent excoriation
2. Potential for injury related to muscle weakness
3. Impaired physical mobility related to muscle weakness
4. Self-care deficit related to severe muscle weakness or flaccid paralysis

38
 5. Anxiety related to decreasing ability to function
a. safety measures
b. ongoing assessment on the ability to function
c. assistance with activities of daily living
d. frequent turning
e. ROM exercises
6. Potential for ineffective breathing pattern related to respiratory muscle weakness
a. assessment of respiratory function
b. positioning
7. Potential for  cardiac output
a. use a cardiac monitor in high-risk, hyperkalemic patients

Medical Therapy
8. Potential for injury related to complication of medical therapy
Careful nursing surveillance:
a. hypoglycemia (insulin & glucose)
b. hypercalcemia (Ca gluconate)
c. metabolic alkalosis (IV bicarbonate)
d. rebound hypokalemia (excessive therapy)
e. inflammation, infection or infiltration (IV therapy)
f. aspiration pneumonitis (oral ion-exchange resin)
g. constipation (oral ion-exchange resin w/o sorbitol)

Note: Kayexalate = ion-exchange resin (Na polysterene sulfonate)

Medical Therapy in K
1. To move K into cells (insulin, glucose, bicarbonate infusion)
2. To counteract the cardiac effects of hyperkalemia (IV Ca gluconate)
3. Remove K from the body (dialysis, diuretics, ion-exchange resins)

CALCIUM BALANCE & IMBALANCES

Facts:
1. Ca ions in the body are mostly located in the bones and teeth.
2. Small amount in cells of soft tissue.
3. Normal concentration range is 4.5 – 5.5 mEq/L (9-11 mg/dl).

Calcium Homeostasis:
1. Major sources of Ca intake:
a. milk
b. dairy products (cheese, cream, yogurt, ice cream)
c. sea foods (clams)
2. Ca is absorbed from the GI tract y active transport mechanism requiring vit. D.
3. Parathyroid hormone increases activation of vit. D.

39
HYPOCALCEMIA
 occurs if the serum Ca level falls below 4.5 mEq/L or if the ionized portion of the serum Ca is
diminished.
 Ionized hypocalcemia : total serum Ca may be normal but ionized Ca concentration will be
below normal.

Causes of Hypocalcemia
1. decreased Ca intake or absorption
2. decreased physiological availability of Ca.
3. increased Ca excretion.
4. calcium loss by abnormal route

Clinical Manifestations
1. Decreased serum Ca (or  ionized Ca & normal total Ca)
2. Paresthesias (digital or perioral) – feeling of numbness or tingling.
3. (+) Chvostek’s sign
 tapping the facial nerve in front of the ear, if the corner of the mouth draws up in a grimace,
sign is (+). Increased neuromuscular irritability is present.
4. (+) Trousseau’s sign
 occluding arterial flow to the hand with a sphygmomanometer cuff for about 3 minutes. If the
hand contorts in a carpal spasm, sign is (+). Indicates increased neuromuscular irritability.
Note: Assessment of both tests frequently in persons at high risk of hypocalcemia (ex. after
thyroid surgery may aid detection and correction of hypocalcemia before life-threatening
laryngospasm or cardiac arrest occurs).
5. grimacing, muscle twitching, cramping
6. hyperactive reflexes
7. carpal, pedal spasm
8. tetany – increase irritability
9. laryngospasm (sudden involuntary muscular contraction of larynx)
10. seizures
11. cardiac arrhythmias

Nursing Dx & Ix
1. Potential for injury related to increased neuromuscular excitability
a. ongoing assessment of neuromuscular function
b. safety measures
c. decreasing environmental stimuli
d. provide seizure precautions
2. Potential for ineffective breathing pattern related to laryngospasm
a. prepare for rapid access to tracheostomy equipment

For patients with paresthesia / muscle cramps:

3. Sensory alteration related to increased neuromuscular irritability
a. explanation of the cause of these unusual sensations
b. patient need to be told that steps are being taken to correct the underlying problem.

For patients with respiratory alkalosis that results from hyperventilation:

a. Position that will not put pressure on efferent nerves (crossing the legs at the knee).

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 4. Knowledge deficit related to hypocalcemia
a. individualized teaching about risk factors and prevention in the future.

Medical Therapy and Collaborative Interventions

 replacement of Ca (oral or IV)

5. Potential for injury related t complications of IV Ca replacement

Potential problems:
a. cardiac arrhythmias (therapy too rapid)
b. rebound hypercalcemia (therapy excessive)
c. inflammation, infection or infiltration
d. tissue sloughing (after Ca infiltration)
Note: oral Ca salts are often administered w/ Vit. D

6. Potential alteration in bowel elimination related to constipation.

HYPERCALCEMIA
 serum Ca concentration exceeds 5.5mEq/L.
 excess Ca in plasma may come from the bones or from an external source

Causes of hypercalcemia
1. increased Ca intake or absorption
2. release of Ca from bone
3. decrease Ca excretion

Clinical Manifestations
1.  serum Ca
2. anorexia
3. nausea, emesis
4. constipation
5. abdominal pain
6. polyuria
7. renal calculi
8. fatigue
9. muscle weakness
10. impaired reflexes
11. headache
12. confusion, lethargy
13. personality change
14. psychosis
15. cardiac arrest
16. ECG changes: shortened QT interval

Nursing Dx & Ix
1. Alteration in Bowel Elimination related to constipation
a. bowel management techniques
2. Potential for alteration in nutrition less than body requirements related to nausea and
anorexia

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 a. measures to reduce nausea
b. provide appetizing foods
3. Potential for aspiration of vomitus
a. positioning on the side.
4. Potential for injury related to fatigue
a. spacing activities
b. scheduling rest periods
5. Potential for injury related to pain
a. pain management or relief measures
6. Self-care deficit related to muscle weakness
7. Decreased level of consciousness
a. providing necessary care
8. Potential for injury related to  level of consciousness
a. safety measures
b. ongoing assessment
9. Alteration in thought processes
10. Impaired social interaction
a. explain effects of Ca on personality and thought processes to significant
others and friends.
11. Potential for pain related to renal calculi
12. Potential for impaired urinary elimination related to renal calculi
a. encouraging the intake of 3-4 L of fluid per day to keep urine diluted
b. provide measures in acidifying urine (ex. restricting dairy products and Ca-rich foods)
c. prevention of UTI (which tends to alkalinize urine).Interventions include:
1. careful catheter care
2. palpation for bladder distention
3. turning immobile patients frequently to avoid urinary stasis
13. Potential for injury related to risk of pathological function
a. pt. must be turned and transferred with very gentle care

Notes:
1. Prune, cranberry juice or an acid ash diet are commonly used to acidify the urine.
2. If hypercalcemia is caused by Ca withdrawal from bones (as in malignancy), bones may be
weakened.
3. Hypercalcemia potentiates digitalis; watch fro digitalis toxicity in patients taking digitalis who
become hypercalcemic.
4. Thiazide diuretics decrease Ca excretion, they should be withheld if Ca develops.

Medical Therapy and Collaborative Interventions

1. Infusion of IV 0.9% Saline to induce saline diuresis
2. Calcitonin may be used to  plasma Ca rapidly in a Ca “E”

14. Potential for injury related to complications of therapy for hypercalcemia

Potential Complications:
1. ECF volume excess (IV saline)
2. inflammation, infection, infiltration (any IV agent)
3. hypokalemia (diuretic therapy)
4. hypersensitivity reaction (calcitonin)

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 5. diarrhea (diphosphonates)
6. nausea,vomiting (plicamycin)
7. bone marrow suppression, liver damage, renal damage (plicamycin)

PHOSPHATE BALANCE AND IMBALANCES

 an anion (negatively-charged)
 integral part of bones and are also abundant inside cells
 normal serum PO4 concentration range is 2.5 – 4.5 mg/dl
 serum PO4 tends to decrease with age in both men and women.

Phosphate Homeostasis:
1. PO4 absorption occurs in the small intestine
2. may be affected by vit. D
3. Mg ions, Al ions diarrhea decrease the absorption of PO4 from intestinal tract
4. PO4 distribution between the ECF and the bones is under the influence of parathyroid
hormone which promotes bone resorption
5. PO4 excretion occurs primarily in urine and feces
6. Parathyroid hormone increases renal excretion of PO4

HYPOPHOSPHATEMIA
 serum PO4 concentration drops below 2.5 mg/dl
 mild hypophosphatemia is often asymptomatic
 if serum PO4 level falls below 1.0 mg/dl, severe symptomatic hypophophatemia occurs which
is serious condition

Causes of Hypophosphatemia
1. decreased PO4 intake or absorption
2. movement of PO4 into cells
3. increased PO4 excretion
4. PO4 loss through abnormal route

Clinical Manifestations
1. serum PO4 below 1 mg/dl
2. anorexia, nausea
3. malaise
4. decreased reflexes
5. muscle weakness, severe debility
6. myalgia
7. bone pain (with long-term antacid overuse)
8. irritability, apprehension
9. paresthesias
10. confusion
11. stupor
12. seizures
13. coma

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Laboratory Values
a. alkalosis ( in pH esp. respiratory alkalosis)

Nursing Dx & Ix
1. Potential for injury related to decreased level of consciousness
a. safety measures
b. ongoing assessment
2. Ineffective breathing pattern related to respiratory muscle weakness
a. careful monitoring
b. semi-Fowler’s positioning
3. Self-care deficit related to LOC and severe muscle weakness
a. frequent turning
b. skin care
c. seizure precautions may be necessary

Medical Therapy & Collaborative Interventions

1. If hypophosphatemia is mild and nutrients are being ingested, the plasma PO4 level may be
monitored and allowed to return to normal spontaneously as precipitating factors are removed.
2. In severe symptomatic hypophosphatemia, PO4 replacement in IV is begun, oral replacement
may follow.

4. Potential for injury related to complications of IV PO4

Potential problems:
a. hypocalcemia
b. rebound hyperphosphatemia
c. inflammation, infection, infiltration
Note:
 Monitor the patient for increased neuromuscular irritability associated with hypocalcemia
because IV PO4 may decrease the plasma Ca concentration rapidly.

HYPERPHOSPHATEMIA
 serum PO4 level above 4.5 mg/dl
 major problem with excess PO4 in the blood is its interaction with Ca ions

Causes of Hyperphosphatemia
1. increased PO4 intake
2. release of PO4 from cells
3. decreased PO4 excretion

Clinical Manifestations
1. serum Ca level falls as serum PO4 rises
2. increased neuromuscular excitability
3. conjunctivitis (eye)
4. band keratopathy (eye)
5. pruritus (skin)
6. acute renal failure (kidney)
7. arthritis (joints)

44
  the serum Ca level does not fall resulting to the precipitation of CaPO4 salts in soft tissues f
the body.

Lab. Values
1. plasma Ca level decreases
2. hyperkalemia
3. hypermagnesemia
4. metabolic acidosis
5.  BUN
6.  creatinine

Nursing Dx & Ix
If the plasma Ca level does not decrease as the plasma level rises, the nursing diagnosis is:
1. Potential for injury related to CaPO4 precipitation in the urinary tract
a. increasing the patients fluid intake (to dilute urine)
C/I: Not to be used in patients with oliguria or a prescribed fluid restriction

If CaPO4 precipitates in the skin , the applicable diagnosis is:

2. Alteration in comfort related to pruritus
a. fingernails must be manicured smoothly to help prevent skin excoriation from scratching

Recurrent episodes of hyperphosphatemia in pt. with CRF may lead to one of the following nursing
diagnosis:
3. Knowledge deficit regarding sources of PO4 intake
4. Noncompliance with PO4 binder therapy
a. individualized teaching or exploring barriers to compliance

Medical Therapy and Collaborative Interventions

1. Restriction of dietary PO4.
2. Often fluid administration to increase urinary PO4 excretion.
3. Patients in chronic renal failure are given PO4 binder therapy.
 aluminum ions in aluminum antacids bind PO4 ions in the GI tract, preventing their
absorption
4. Explain that antacids need to be taken during rather that after meals to mix the PO4 binder
with food.
5. Remind patients not to use Mg – Al antacids; Mg is C/I in patients with renal failure.

MAGNESIUM BALANCE & IMBALANCES

 most of Mg ions in the body are located in the bones

 rest of Mg is intracellular especially in liver and skeletal muscle
 small amount of Mg n the blood
 normal serum Mg range is 1.5 – 2.5 mEq/L for adults of all ages

Foods with High Mg Content

1. whole grain cereals
2. dark green vegetables

45
 3. dried beans and peas
4. soy products
5. nuts (esp. cashews & almonds)
6. peanut butter
7. cocoa, chocolate
8. bananas
9. egg yolk
10. sea salt

HYPOMAGNESEMIA
 serum Mg concentration below 1.5mEq/L

Causes of Hypomagnesemia
1. decreased Mg intake or absorption
2. decreased physiological availability of Mg
3. increased Mg excretion
4. magnesium loss by abnormal route

Clinical Manifestations
1. serum Mg level  normal
2. insomnia
3. hyperreflexia
4. (+) Chvostek’s sign
5. (+) Trosseau’s sign
6. leg & foot cramps
7. grimacing
8. dysphagia
9. ataxia (voluntary incoordination of muscular movement)
10. nystagmus
11. tetany
12. seizures & LOC
13. extreme confusion
14. cardiac arrhythmias
15. ECG changes: ST & T wave abnormalities

Laboratory Values
1. abnormal plasma concentration of other electrolytes
2. hypokalemia (most common)
3. hypocalcemia
4. hypophosphatemia
5. hyponatremia

Medical Therapy & Collaborative Interventions

1. Mg replacement (oral or IV)
Diagnoses:
1. Potential alteration in bowel elimination related to diarrhea
2. Potential for injury related complications of IV Mg therapy

46
 Potential problems:
a. flushing, sweating (infusion too rapid;  the rate)
b. rebound hypermagnesemia (therapy excessive)
c. inflammation, infection, or infiltration
Notes:
1. IV SO4 must be administered carefully.
2. Check for adequate renal function before administering parenteral Mg.
3. It is advisable to test the patellar reflexes before administering each dose. If these reflexes
diminish or disappear, serum Mg concentration should be rechecked because it may have
elevated.

HYPERMAGNESEMIA
 serum Mg concentration above 2.5 mEq/L

Causes of Hypermagnesemia
1. increased Mg intake or absorption
2. shif of Mg from bones into blood
3. decreased Mg excretion

Clinical Manifestations
1. decreased neuromuscular excitability
2. increased serum Mg concentration
3. hypotension
4. flushing, diaphoresis
5. drowsiness, lethargy
6. diminished deep tendon reflexes
7. flaccid paralysis
8. respiratory depression
9. bradycardia
10. cardiac arrhythmias
11. cardiac arrest
12. ECG changes

Nursing Dx & Ix
1. Alteration in comfort related to flushing & diaphoresis
a. explanation of cause
b. skin care
2. Potential for injury related to decreased LOC
a. safety measures
b. ongoing assessment
3. Self-care deficit related to LOC and flaccid paralysis
a. providing necessary care
4. Alteration in mobility related to flaccid paralysis
a. frequent turning
b. skin care
5. Ineffective breathing pattern related to respiratory depression
a. careful monitoring
b. semi-Fowler’s positioning

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 6. Potential for decreased cardiac output related to cardiac arrhythmias or arrest
a. careful monitoring

Patients with CRF may be diagnosed as:

7. Knowledge deficit regarding sources of Mg intake or noncompliance with Mg restriction
a. dialysis

Medical Therapy & Collaborative Interventions

1. Removal of excess Mg from plasma.
a. If renal function is normal, this is often accomplished by administering large amounts of
fluid to  renal Mg excretion.
b. In renal failure, hemodialysis may be used to remove excess Mg from plasma.
c. In severe hypermagnesemia, Ca salts may be administered /IV to counteract the
cardiotoxic effects of excess extracellular Mg.
Possible Complication:
1. hypercalcemia
2. tissue sloughing (infiltrates)
3. digitalis toxicity (if receiving digitalis therapy)

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 ACID-BASE IMBALANCE

Important Facts:
 Hydrogen ions are vital to life & health.
 The concentration of hydrogen ions in the body is less than that of other ions (0.00004mEq/L)
 Hydrogen ion concentration is expressed as pH
 Information about a patient’s acid-base status is obtained by testing a sample of arterial blood
(arterial blood gas) for the following values:
a) pH (normal 7.35-7.45) – measure of hydrogen ion concentration.
b) pCO2 (normal 36-44mmHg) – partial pressure of carbon dioxide
c) Bicarbonate (normal 22-26mEq/L) – sometimes reported as carbon dioxide content.
 A reading less than 7.35 is present in acidosis
 Reading is greater than 7.45 is present in alkalosis.
 Limits of pH compatible with life are 7.0 – 7.8

Mechanisms regulating acid-base balance

A) Chemical buffers in cells and ECF

 instantaneous action
 combine acids or bases added to the system to prevent marked
changes in pH
B) Respiratory System
 minutes to hours action
 controls CO2 concentration in ECF by changes in rate and depth of
respiration.
C) Kidneys
 hours to days action
 increases or decreases quantity of NaHCO3 in ECF
 combines HCO3 or H with other substances and excretes them in
urine.

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ACID BASE MNEMONIC (ROME)

R Respiratory
O Opposite
pH  pCO2   ALKALOSIS
pH  pCO2   ACIDOSIS
M Metabolic
E Equal
pH  HCO3   ALKALOSIS
pH  HCO3   ACIDOSIS

ACIDOSIS
 is the presence of any process that tends to decrease the pH of blood
below the normal range.

A. Respiratory Acidosis (Carbonic Acid Excess)

Causes:
1. General Etiology: Decreased Gaseous Exchange
a. Decreased alveolar ventilation
b. COPD
c. Emphysema
d. Severe asthma
e. Sleep apnea (obstructive type)
f. Atelectasis
g. Pneumonia
h. Adult respiratory distress syndrome
i. Pulmonary edema
j. Hypoventilation by way of mechanical ventilator
2. General Etiology: Impaired neuromuscular function of chest
a. Chest injury
b. Surgical incision (pain limits respirations)
c. Poliomyelitis
d. Guillain-Barre syndrome
e. Respiratory muscle fatigue
f. Myasthenia gravis
g. Hypokalemia
h. Kyphoscoliosis
i. Pickwickian syndrome (obesity limits chest expansion
3. General Etiology: Suppression of neural Ventilatory Mechanisms in Brain Stem
(Medulla)
a. Narcotics
b. Barbiturates

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 c. Sleep apnea (central type)

Clinical Manifestations:
1. Increased pCO2
2. Headache
3. Blurred vision
4. Disorientation
5. Tachycardia
6. Cardiac arrhythmias
7. Lethargy
8. Somnolence

Laboratory values
Partially Fully
Uncompensated Compensated Compensated
Respiratory Respiratory Respiratory
Acidosis Acidosis Acidosis
pCO2 Increased Increased Increased
HCO3 Normal Increasing Increased
[HCO3] Normal (less than 20/1) Increasing Increased (equals 20/1)
[H2CO3] Increased Increased Increased
pH Decreased Moving toward normal Normal

Medical Therapy and Collaborative Ix

1. Improvement of ventilation through the administration of bronchodilators or through
mechanical ventilator.
2. For severe type, infusion of NaHCO3 to raise pH toward normal.

B. Metabolic Acidosis (Noncarbonic Excess)

 occurs when there is an accumulation of any other kind of acid in
the bloodstream such as lactic, sulfuric, citric, oxalic, acetylsalicylic, and beta-hydroxybutyric
acids.

Causes:
1. General Etiology: Acid Accumulation by Ingestion of Acid or Acid Precursors
a. Aspirin
b. Methanol
c. Ethylene glycol
d. Paraldehyde
e. Boric acid
f. Elemental sulfur
g. Ammonium chloride

2. General Etiology: Acid Accumulation by Increased Production of Metabolic Acids

a. Hyperthyroidism
b. Hypermetabolic state after burns or trauma
c. Lactic acidosis
d. Shock

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 3. General Etiology: Acid Accumulation by Utilization of Abnormal or Incomplete
Metabolic Pathways
a. Diabetic ketoacidosis
b. Alcoholic ketoacidosis
c. Starvation ketoacidosis

4. General Etiology: Acid Accumulation by Impaired Acid Excretion

a. Oliguric renal failure
b. Severe hypovolemia
c. Shock
d. Renal tubular acidosis
e. Hypoaldosteronism

5. General Etiology: Primary Decrease of Bicarbonate

a. Urinary Route: Renal tubular acidosis
b. Gastrointestinal Route:
1. severe diarrhea
2. intestinal decompression
3. ureterosigmoidostomy
4. fistula drainage
5. vomiting of intestinal contents
6. cholestyramine therapy

Clinical Manifestations:
1. decreased bicarbonate ion concentration
2. hyperventilation (compensatory mechanism)
3. headache
4. abdominal pain
5. confusion
6. drowsiness
7. lethargy
8. stupor
9. coma
10. cardiac arrhythmias

Laboratory values

Partially Fully
Uncompensated Compensated Compensated
Metabolic Metabolic Metabolic
Acidosis Acidosis Acidosis
pCO2 Normal Decreasing Decreased
HCO3 Decreased Decreased Decreased
[HCO3] Decreased (less than 20/1) Decreased Decreased(equals 20/1)
[H2CO3] Normal Decreasing Decreased
pH Decreased Moving toward normal Normal

52
Medical Therapy and Collaborative Ix
1. Elevation of pH through IV infusion of NaHCO3.
2. Oral bicarbonate or citrate may be administered in chronic metabolic acidosis.

ALKALOSIS
 a process that tends to increase the pH of blood above the normal
range.
A. Respiratory Alkalosis (Carbonic Acid Deficit)
Causes:
1. General Etiology: Hyperventilation
a. anxiety or fear
b. pain
c. prolonged crying and gasping
d. hypoxemia
e. some brain injuries
f. hyperventilation by means of mechanical ventilator
g. stimulation of neural ventilatory mechanisms in brain stem (medulla)
1. high fever
2. meningitis
3. encephalitis
4. salicylates (overdose)
5. progesterone (high levels)
6. gram-negative septicemia

Clinical Manifestations:
1. decreased pCO2
2. diaphoresis
3. lightheadedness
4. paresthesias (fingers, toes, circumoral)
5. muscle cramps
6. (+) Chvostek’s sign
7. (+) Trousseau’s sign
8. carpopedal spasm
9. tetany
10. syncope
11. cardiac arrhythmias

Laboratory values
Partially Fully
Uncompensated Compensated Compensated
Respiratory Respiratory Respiratory
Alkalosis Alkalosis Alkalosis
pCO2 Decreased Decreased Decreased
HCO3 Normal Decreased Decreased
[HCO3] Normal (greater than 20/1) Decreasing Decreased (equals 20/1)
[H2CO3] Decreased Decreased Decreased
pH Increased Moving toward normal Normal

53
Medical Therapy and Collaborative Ix
1. Correcting the underlying disorder and monitoring for its effectiveness and potential
complications.

B. Metabolic Alkalosis (Noncarbonic Acid Deficit)

 a deficit of any acid except carbonic acid.

Causes:
1. General Etiology: Decrease of Acid
a. Gastrointestinal route
1. emesis
2. gastric suction
b. Urinary route
1. hyperaldosteronism
2. glucocorticoid excess
3. chronic excessive ingestion of black licorice
4. diuretic therapy
c. Acid movement into cells
1. hypokalemia

2. General Etiology: Increase of Base (Bicarbonate Ions)

a. excess infusion or ingestion of NaHCO3
b. excess administration of lactate or acetate (bicarbonate precursors)
c. massive blood transfusion

Clinical Manifestations:
1. Initial disorder
a. nausea, emesis
b. paresthesias
c. tetany
d. seizures
2. Profound disorder
a. confusion
b. lethargy
c. coma

Laboratory values
Partially
Uncompensated Compensated
Metabolic Metabolic
Alkalosis Alkalosis
pCO2 Normal Increasing Full compensation for
HCO3 Increased Increased metabolic alkalosis is
[HCO3] Increased (greater than 20/1) Increased limited by the body’s

54
[H2CO3] Normal Increasing need for oxygen
pH Increased Moving toward normal

Medical Therapy and Collaborative Ix

1. Directed toward treating the original cause of the imbalance and enhancing the renal
excretion of bicarbonate ion to correct the imbalance.
2. If profound, dialysis may be instituted.

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