FLUID AND ELECTROLYTES:

Balance and Distribution

STARLING LAW OF THE CAPILLARIES
Whether fluids leave filtration or enter reaborption capillaries depends on how the pressures in the
capillary and interstitial spaces relate to one another.
Volume re absorbed is similar to volume filtered A net equilibrium.
Regulates relative volumes of blood and interstitial fluid.
CAPILLARY EXCHANGE
The 5% of the blood in systemic capillaries the bulk of blood that exchanges materials with systemic tissue
cells.
Substances that pass through thin capillary walls into interstitial fluid and then into cells are:
a. Nutrients
b. Oxygen
Substances that are secreted by tissue cells and are removed from the are:
a.
Wastes
b.
Carbon dioxide
FLUID AND ELECTROLYTES
60% of body consist of fluid
Intracellular space
75 %
Fluids inside the cells.
Internal aqeous medium for cellular chemical function.
Extracellular

space
25 %
Fluids outside the cells.
Maintains blood volume.
Transport system to and from the cell.

a. Interstitial
Contains fluids that surrounds the cells
e.g. Lymph
b. Intravascular
Fluid within the blood vessels.
c. Transcellular
Smallest division of ECF comapartments.
e.g. Cerebrospinal fluid, synovial, intraocular and pleural fluids, sweat and digestive secretions.
BODY WATER
Distributions vary with age and sex.
a. Infant 80 %
b. Male - 60 %
c. Female 50 %
(Fat is water free. Females have more adipose tissues, so they have lesser percentage of body water.)

FUNCTIONS OF BODY WATER

Maintains ECF.
Maintains ICF.

Maintains
the
normal
temperature.
Elimination of waste products.

ELECTROLYTES
Chemical compounds in solution that have the ability to conduct an electrical current.
Are substances that, when in solution separate into electrically charged particles called Ions.
Break into charged particles called
Ions.
Positively charged ions: CATIONS.
Negatively charged ions: ANIONS.

FUNCTION OF ELECTROLYTES
Promote neuromuscular irritability.
Maintain body fluid volume and osmolarity.
Distribute water between fluid compartments.

EFC:
MAJOR CATIONS: Sodium
MAJOR ANIONS: Chloride
IFC:
MAJOR CATIONS: Potassium
MAJOR ANIONS: Phosphate

body

 Regulate acid base imbalance.

ORGAN AND GLAND INVOLVEMENT IN FLUID REGULATION
1. Kidney
Regulates ECF volume and osmolality by selective retention and excretion of body fluids.
Regulation of electrolyte levels in the ECF by selective retention of needed substances and excretion of
unneeded substances.
Regulation of pH of the ECF by retention of hydrogen ions.
Excretion of metabolic waste and toxic substances.
2. Heart and Blood vessels
Pumping action of the heart circulates blood through the kidneys under sufficient pressure to allow for
urine formation.
3. Lungs
Through the exhalation the lungs remove water.
Maintains acid base balance.
4. Pituitary
Release ADH that retains water.
Maintaining the osmotic pressure of the cells by controlling the retention and excretion of water by the
kidneys and by regulating blood volume.
5. Adrenal
Secretes Aldosterone that causes sodium retention and potassium loss.
6. Parathyroid
PTH influences bone reabsorption, calcium absorption from the intestine and calcium reabsorption from
the tubules.
NORMAL FLUID INTAKE AND LOSS IN ADULTS
Intake

Water in food
Water from oxidation
Water as liquid

Output

= 1,000 mls
= 300 mls
= 1,200 mls

TOTAL : 2,500 mls

Skin
Lungs
Feces
Kidneys

= 500 mls
= 300 mls
= 150 mls
= 1,500 mls
TOTAL : 2,500 mls

MAINTAINING BODY FLUID BALANCE

1. Antiduiretic Hormone
Restore blood volume by reducing diuresis and increasing water retention.
Hypothalamus senses low volume and increased serum osmolality and signals the pituitary gland.

Pituitary gland secretes ADH into the blood stream

Kidneys retain water

Water retention

Increased blood volume and serum osmolality

2. Renin angiotensin aldosterone system
Maintain balance of sodium and water.
Blood flow to the glomerulus

Juxtaglomerular cells secretes renin into the blood stream

Renin travels to the liver

Renin convert angiotensinogen in the liver to angiotensin I

Angiotensin I travels into the lungs

Angiotensin I is converted in the lungs into the angiotensin II


Angiotensin II travels into the adrenal glands

Angiotensin II stimulates the adrenal glands to produce aldosterone

3. Aldosterone
Acts to regulate fluid volume.
Angiotensin II stimulates the adrenal gland to release aldosterone

Aldosterone cause the kidney to retain sodium and water

Sodium and water retention leads to increase in fluid volume and sodium levels
TRANSPORT MECHANISM
A. Passive Transport Mechanism ( ECF
ICF)
No energy required to accomplish the movement of substances across a cell membrane.
1. Diffusion
Substances move from an area of higher concentration to and area of lower concentration.
2. Osmosis
Water moves from an area of higher concentration to an area of lower concentration.
Is the diffusion of water caused by fluid gradient.
Tonicity
Is the ability of solutes to cause osmotic driving force that promotes water movement from one
compartment to another.
Osmotic Pressure
Is the amount of hydrostatic pressure needed to stop the flow of water by osmosis.
Oncotic Pressure
Is the osmotic pressure exerted by proteins (e.g. albumin).
Osmotic Diuresis
Is the increase in urine output caused by the excretion of substance.
Filtration
Movement of water and solutes from an area of high hydrostatic pressure to an area of low
hydrostatic pressure.
Osmolality
Reflects the concentration of fluid that affects the movements of water between fluid
compartments by osmosis.
B. Active Transport Mechanism (IVC
ISC)
Requires energy to move molecules and ions from an area of lower concentration to higher concentration.
1. Sodium Potassium Pump
Moves sodium from the inside the cells to the outside and potassium moves from the outside to the
cell inside.
Sodium concentration is higher in ECF than ICF.
Sodium enters cell by diffusion.
Potassium exits cell into ECF
2. Pinocytosis
Tiny vacuoles take droplets of fluid containing dissolve substances into the cell.
CONCEPTS AND PRINCIPLES
a. Sodium and Water
Thirst. The major control of actual fluid intake.
Kidney. Major organ controlling output.
ADH (Antiduiretic Hormone). Caused increased water reabsorption in the distal convoluted tubules and
collecting ducts.
RAAS (Renin Angiotension Aldosterone System).
The osmolality of body fluids depends predominantly on Sodium and its associate anions.
Osmolality is an expression of concentration of solution in terms of 1,000 of water.
Osmolarity is an expression of concentration of solution in terms of 1,000 mL. of water.
b. Potassium
The major ICF cation and regulates intracellular osmolality.
Important in the conduction of nerve impulses and promotion of proper skeletal and cardiac muscle
activity.

 The major excretion site of excess potassium is the kidney.

Aldosterone
Increased the amount of K secreted of K from distal tubules s.K.
Hydrogen Ion
Hydrogen Ion concentration
Hydrogem Ion (alkalosis) K excretion hypokalemia
Hydrogen Ion (acidosis)

K Excretion

H Ions enter the cells K

shift into the ECF.

Hyperkalemia
c. Calcium
Promotion of neuromuscular irritability and muscular contrations.
Calcium and Phosphorus: 99% found in bones and teeth, 1% in blood.
Calcium and Phosphorus have inverse relationship.
If both are elevated insoluble precipitate.
total CHON and albumin - total s.Ca.
Parathormone s. Ca PTH release Ca is withdrawn from the bones.
s. Ca.

Ca absorption in GIT
Ca reabsorption in renal
tubules

Vitamin D promotes absorption of Calcium from GIT.

Thyrocalcitonin s. Ca Thyrocalcitonin release inhibits release of Ca from bones s. Ca.

FLUID VOLUME DISTURBANCE

HYPOVOLEMIA (Fluid Volume Deficit)
Loss of body fluid or the shift of fluids into 3rd space.
Isotonic fluid loss from the extracellular space.
Risk Factors

Inadequate or Reduced fluid intake

Third space fluid shift (edema and effusion)
Electrolyte and acid base imbalances
Abdominal surgery
Diabetes Mellitus
Excessive diuretic therapy
Excessive laxative use

Excessive sweating
Fever
Hemorrhage
Nasogastric drainage
Renal failure with increased urination
BUN will be elevated due to low volume
(Normal BUN = 10 -25)
Vomiting and diarrhea

Signs and symptoms

a. Increased heart rate
b. Orthostatic hypotension
c. Restlessness / Anxiety

d. Delayed capillary refill

e. Cool, Pale skin

Danger Signs
a.
b.
c.
d.
e.
f.

Deterioration in mental status

Thirst
Tachycardia
Delayed capillary refill
Orthostatic hypotension progressing to mark
hypotension
Urine output drops below 10 mL / hr.

g.
h.
i.
j.
k.
l.

Diagnostic test
1. Normal or high serum sodium > 145 mEq/L

Cool, Pale skin over the arms and legs

Weight loss
Flat jugular veins
Decreased central venous pressure
Weak or absent peripheral pulses
Shock

2. Hemorrhage decreased hemoglobin

hematocrit
3. Elevated creatinine and BUN ratio

and

4. Increase urine specific gravity

5. Increased serum osmolality

Medical Management
1.
2.
3.
4.
5.

IV fluids replacement
Blood transfusion
Vasopressors such as dopamine
Oxygen therapy
Surgery

Nursing Intervention
1.
2.
3.
4.
5.
6.
7.
8.
9.

Monitor I and O frequently.

Normal urinary output = 30 60 cc / hr.
Check O2 sats and draw blood gases.
Auscultate lungs (side to side).
Check temperature distal from heart.
Give a fluid bolus as ordered.
Ensure patient airway.
Apply oxygen as ordered.
Lower the head of the bed to show a declining
blood pressure.

10. Bleeding apply direct continuous pressure to

the area and elevate it.
11. Monitor patients mental status and vital signs.
12. Monitor quality of peripheral pulses and skin
temperature.
13. Encourage to drink fluid appropriately.
14. Weigh patient daily to monitor the progress of
treatment.
15. Provide effective skin care to prevent skin
breakdown.

HYPERVOLEMIA (Fluid Volume Excess)

Excess of isotonic fluid in the intravascular and interstitial spaces third spacing.
Isotonic fluid retention is primarily related to renal failure.
Excess of isotonic in the extracellular compartment.
Risk Factors
Fluid overload such as IV fluid replacement and
Blood or plasma replacement
High intake of dietary sodium
Heart failure
Renal failure
Cirrhosis of the liver
Nephrotic syndrome

Corticosteriod therapy
Hyperaldosteronism
Low intake of dietary protein
Remobilization of fluids after burn treatment
Consumption of excessive amount of sodium

Signs and symptoms

a.
b.
c.
d.
e.

Increased cardiac output

Rapid and bounding pulse
Crackles
Tachycardia
Increase BP , pulse pressure and CVP

f.
g.
h.
i.
j.

Increased weight
Increased urine output
Shortness of breath and wheezing
Distended neck veins
Edema

Diagnostic Findings
a.
b.
c.
d.
e.

Low hematocrit
Low serum potassium and BUN levels
Decreased serum osmolality
Low O2 level
Pulmonary congestion through X - ray

Medical Management
1.
2.
3.
4.

Restriction of fluid and sodium intake

Diuretic
Morphine and nitroglycerine
Digoxin

5. O2 and bed rest

6. Hemodialysis / continuous renal replacement
therapy (CRRT)

Nursing Intervention
1. Assess patients vital signs and hemodynamic
status.
2. Monitor for respiratory patterns for worsening
distress.
3. Watch for distended veins in hands and neck.
4. Record intake and output hourly.

5. Listen to breath sounds regularly to assess for

pulmonary edema.
6. Follow ABG result and watch for a drop in O2
level or changes in acid base balance.
7. Raise the head of the bed.
8. Restrict fluid intake.

9. Maintain IV access for administration of

11. Offer emotional support.
medications.
10. Weigh the patient daily.
HYPERALDOSTERONISM
Iatrogenic hypervolemia: Mistake made by Health Care Staff . Too much IV fluids!
ELECTROLYTES AND ITS IMBALANCES
A. Sodium (Na) : 135 145 mEq/L
Main extracellular fluid cation.
Helps govern normal ECF osmolality.
Must be present for glucose to be transported to the cells.
Helps maintain acid base balance.
Actives nerve and muscle cells.
Sodium and Potassium have inverse relationship.
Necessary for neuromuscular functioning.
Determines intracellular reactions.
Maintains acid base balance.
Dietary Sources
Canned goods

Cheese

Ketchup

Processed meats

Table salts
Salty snacks foods
Seafoods

HYPONATREMIA
Sodium loss or water excess
Etiology
Treatment with diuretics
Restricted sodium intake
Loss from GI or biliary drainage and draining
fistulas
Decreased
aldosterone
secretion
(Addisons
disease)

Trapping of sodium and water

Edema, ascites, burns or small bowel obstruction
Diaphoresis warm climate, exercise, fever, and
salt wasting nephritis

Sign and symptoms ( ECF, ICF)

a.
b.
c.
d.
e.

Headache
Muscle weakness
Fatigue and apathy
Postural hypotension
Anorexia, nausea and vomiting

f.
g.
h.
i.

Abdominal cramps
Weight loss
Feelings of apprehension
Seizures and coma

Collaborative Management
1.
2.
3.
4.

Treatment of shock
Replace other electrolytes depleted (K, Ca, HCO3)
Salt, salty foods in diet
Safety precaution (e.g. Use of side rails and supervision of ambulation)

HYPER NATREMIA
Na and water excess edema: Excess Na in relation to water in ECF Hypernatremia
Etiology
More water than Na is lost from the body such as
hyperventilation and diarrhea.
High Sodium intake
Salt tablets

Rapid infusion of saline or IV

Water deprivation
Na ECF osmolality ICF moves into ECF
ICF dehydration

Signs and symptoms

a.
b.
c.
d.

Extreme thirst
Dry, sticky mucous membrane
Oliguria
Firm, rubbery tissue turgor,
agitation
e. Red, dry, swollen tongue

f.
g.
h.
i.
j.

excitement,

Tachycardia
Fatigue
Restlessness
Disorientation
Hallucination

Collaborative Management
1.
2.
3.
4.
5.
6.

Monitor I and O.
Restrict sodium in diet.
Monitor behavioral changes.
Increase oral fluids or D5W / IV.
Diuretics
Dialysis

B. Potassium (K) : 3.5 5 mEq/L

Main intracellular fluid cation.
Regulates cell excitability.
Excitability of nerves and muscles.
Control ICF osmolality and consquenly.
ICF osmotic pressure.
Maintains acid base balance and normal kidney function.
K deficit Alkalosis
K excess Acidosis
Anabolism or glycogenesis: K ENTERS THE CELL
Catabolism (Trauma, Dehydration, Starvation): K LEAVES THE CELL
Dietary Sources
Banana
Dried fruits (raisin, prunes)
Orange
Raw carrot
Raw tomato
Baked potato
Melon (Cantaloupe)
Watermelon
HYPOKALEMIA
DECREASED INTAKE
Food and fluids as in
starvation.
Failure to replace losses.

INCREASED LOSS
Aldosterone
Gastrointestinal losses
Potassium losing diuretics
Loss from cells as in trauma, burns

SHIFT OF POTASSIUM INTO CELLS

(No change in total body
potassium)
Treatment of diabetic acidosis
Metabolic alkalosis

HYPOKALEMIA

GIT

CNS

MUSCLE

CV

KIDNEY

Anorexia
Nausea
and
vomiting
Abdominial
distention

Paralytic ileus

Lethargy
Diminished
deep
tendon
reflexes
Confusion
Mental
depression

Weakness

Flaccid paralysis
Weakness
of
respiratory muscles

Respiratory
arrest
(Probably cause of
death
in
hypokalemia)

Decreased
in
standing BP
Dysrhythmias

ECG changes

Myocardial
damage

Cardiac Arrest

Anorexia

Capacity
concentration
waste

Water loss

Thirst

Kidney Damage

Collaborative Management
1. Potassium rich foods.
2. Potassium supplement:
ORAL: K durule tab 1 3 tabs daily.
IV incorporation / slow drip.

3. Potassium sparing diuretics.

HYPERKALEMIA
EXCESS INTAKE
Dietary intake in excess of
kidneys ability to excrete.
Excess
parenteral
administration.

DECREASED LOSS
Potassium sparing
Diuretics
Renal failure
Adrenal insuffiency

SHIFT OF POTASSIUM OUT

OF CELLS
Extensive trauma
Crushing injuries
Metabolic acidosis

HYPERKALEMIA

GIT
Nausea
vomiting

and

Diarrhea Colic

CNS

MUSCLES

Numbness

(Early)
Irritability
(Late)
Weakness

Tingling
sensation

CV

KIDNEY

Conduction
disturbance

Oliguria

Ventricular
fibrillation

Flaccid
Paralysis

Cardiac Arrest

Anuria

Collaborative Management
1. Avoid Potassium rich foods.
2. Promote bedrest.
3. 10 % glucose with regular insulin / IV.

4. Polysterone
sulfonate
(exchange
resin
kayexalate).
5. Ca / IV ( antagonist effect of Potassium).
6. Dialysis

C. Calcium (Ca) : 8.9 10.1 mg/dL

A major cation in teeth and bones.
Equal concentrations in ICF and ECF.
Maintain cell membranes shape.
Acts as an enzyme activator within the
cells.
Aids coagulation.

Two types:
a. Ionized
b. Plasma protein bound

Free ionized calcium is needed for:

a. Blood coagulation
b. Smooth, skeletal and cardiac muscle
function
c. Nerve function
d. Bone and teeth formation

Vitamin D and PTH increases GI calcium

absorption.
Calcitonin = Blood to bone
Parathyroid hormone = Bone to blood.
Dietary Sources
Yogurt, low fat
Milk
Rhubarb
Collard green
Cheese
Tofu
Spinach
Broccoli
Green beans
Carrots

HYPOCALCEMIA

DECREASED IONIZED
CALCIUM
Large transfusion with
citrated
blood
alkalosis

EXCESS LOSS

INADEQUATE
INTAKE

Kidney disease
Draining fistula

Decreased
intake

dietary

DECREASED GI TRACT AND

BONE ABSORPTION
Vitamin D
PTH
Magnesium
Calcitonin

HYPOCALCEMIA

BONES

CNS

OTHER

GI TRACT

MUSCLES

CV

Osteoporosis

Tingling

Dysrhymias

Fracture

Convulsion

Increased
Peristalsis

Nausea and
Vomiting
Diarrhea

Muscle Spasm

Abnormal
deposits of
calcium body
tissue

Tetany

Cardiac Arrest

Increases Calcium blocking effect on cell membrane permeability depressed nerve and muscle
activity.
When a person is immobilized, Calcium leaves the bones and concentrate in ECF precipitates and forms
stones in the kidneys.

Collaborative Management
1.
2.
3.
4.

High calcium diet

Calcium gluconate
Oral calcium salts
Monitor breathing (laryngeal stridor)

5. Vitamin D, PTH supplement

6. Phosphate binder (AL OH)
Phosphate Calcium
7. Safety precaution (seizures may occur).

HYPERCALCEMIA

LOSS FROM BONES

Immobilization
Carcinoma
with
bone
Metastases
Multiple myeloma

EXCESS INTAKE
Calcium diet (especially
milk)
Antacid containing calcium.

INCREASE IN FACTORS CAUSING

MOBILIZATION FROM BONE
Parathyroid hormone
Vitamin D and steroid therapy

HYPERCALCEMIA

KIDNEY

CNS

BONES

MUSCLES

CV

Stones

Deep tendon
reflexes

Lethargy

Coma

Bone pain

Osteoporosis

Fracture

Muscles fatigue,
Hypotonia

Depressed activity

Dysrhythmias

Kidney
Damage

Gastrointestinal
Tract

Cardiac Arrest

Collaborative Management
1. Increased fluid intake (3-4 L/day). To reduce risk of stone formation in the kidneys (Urolithiasis) and relieve
thirst due to polyuria.
2. Acid ash fruit juices (prune juices and cranberry), ascorbic acid. Acidic urine inhibits stone formation in the
kidney.
3. NSS / IV and diuretic. Calcium excretion is promoted by Sodium excretion.
4. Mithramycin (mithracin). It reduces serum Calcium level.
5. Protect from injury to avoid fracture.
D. Magnesium (Mg) : 1.5 2.5 mEq/L
Second most abundant ICF cation.
Essential for neuromuscular function.
Changes in serum Magnesim levels effect other electrolytes.
A leading ICF cation.

Modifies nerve impules transmission and skeletal muscle response.

Excreted primarily by kidneys.

Dietary sources
Green leafy vegetables such as spinach and
broccoli
Avocado
Canned white tuna fish
Low fat yogurt
Cooked rolled oats
Milk

Peas
Potatoes
Pork, Beef and Chicken
Raisins
Peanut butter
Cauliflower

HYPOMAGNESEMIA (Tetany)

s magnesium neuromuscular irritability by acetycholine realease sensitivity of the myoneural

junction.
Calcium Magnesium ; Calcium Magnesium
Hypomagnesemia potentiates action of digitalis

DECREASE INTAKE
Prolonged malnutrition
Starvation

IMPAIRED ABSORPTION FROM GI TRACT

Malabsorption syndromes
Alcohol withdrawal syndrome
Hypercalcemia
Diarrhea
Draining gastrointestinal fistulas

EXCESSIVE EXCRETION
Aldosterone
Condition causing large
losses of urine

HYPOMAGNESEMIA

MENTAL
CHANGES

CNS

Agitation
Depression

MUSCLES

CV

Convulsion

Cramps

Tachycardia

Paresthesias

Spasticity

Hypotension

Tremor

Tetany

Dysrhythmias

Ataxia

Confusion

Collaborative Management
1.
2.
3.
4.
5.

Dietary supplement : Fruit, green vegetables, whole grains, cereal, milk, meat, nuts, and seafoods.
Magnesium sulfate oral / parenteral.
Promote safety, prevention from injury.
Monitor for laryngeal stridor.
Correct underlying cause.

HYPERMAGNESEMIA (Weakness)
Etiology
Renal failure
Diabetic ketoacidosis
Frequent use of magnesiem containing antacids or cathartics.
Magnesium blocks acetylcholine release decreased excitability of muscle
Signs and symptoms
a.
b.
c.
d.

Decreased BP
Thirst, nausea and vomiting
Drowsiness
Loss of DTRs (deep tendon reflexes)

10

Collaborative Management
1. Calcium Gluconate / IV
Antagonist of Magnesium
2. Dialysis if with Renal Failure
3. Correction of underlying cause.
E. Phosphorus (P) : 1.8 2.6 mEq/L
Main ICF anion.
Promotes energy stores and carbohydrates, protein and fat metabolism.
Acts as hydrogen buffer.
Importance
a) Muscle function
d) Compound in RBC transport air
b) Neurologic function
e) Acid base buffer
c) Metabolism of carbohydrates, fats and
f) White blood cells and platelets formation.
protein.
Dietary Sources
Cheese
Nuts and seeds
Dried beans
Organ meat
Eggs
Poultry
Fish
Whole grains
Milk products
HYPOPHOSPHATEMIA
Occurs when serum level falls below 1.8 mEq/L.
Etiology
Shift of phosphorus from extracellular fluid to in
tracellular fluid.
Decrease in intestinal absorption of phosphorus.
Increase loss of phosphorus through kidneys.
Respiratory alkalosis
Insulin transports glucose and phosphorus into the
cells.

Use of antacid / sucralfate

Inadequate Vitamin D.
Chronic diarrhea and laxative abuse.
Decrease dietary intake.
Increase PTH.

Signs and Symptoms

a.
b.
c.
d.
e.

Muscle weakness
Diplopia
Malaise and anorexia
Weakened hand grasp
Slurred speech / dysphagia

f.
g.
h.
i.
j.

Myalgia
Respiratory failure
Paresthesia
Memory loss
Seizures / coma

4.
5.
6.
7.

Monitor rate and depth of respirations.

Monitor for signs of heart failure.
Ensure client maintains bed rest.
Record intake and output.

Medical Management
1.
2.
3.
4.

Phosphorus replacement
High phosphorus diet
Neura Phos and Neura Phos K
IV phosphorus replacement

Nursing Management
1. Monitor for sign and symptoms of this
imbalance.
2. Monitor vital signs.
3. Assess the patients level of consciousness and
neurologic status.
HYPERPHOSPHATEMIA
Occurs when serum phosphorus level exceed 2.6 mEq/L.
Risk Factors
Impaired renal excretion of phosphorus.
Increase dietary intake of phosphorus.

Shift of phosphorus from intracellular fluid to

extracellular fluid.

Signs and Symptoms

11

a. Hypocalcemia
b. Paresthesia
c. Muscle spasm

d. Hyperreflexia
e. (+) chvosteks test and trousseaus sign.
f. Delirium and seizures

Medical Management
1. Reduce phosphorus intake.
2. Aluminum, magnesium, calcium carbonate / acetate.
3. Treat the underlying cause.
Nursing Intervention
1. Monitor vital signs.
2. Monitor fluid intake and output.
F. Chloride (Cl) : 96 106 mEq/L
Main ECF anion.
Helps maintain normal ECF osmolality.
Affects body pH.
G. Bicarbonate (HCO3) :
Present in ECF.
Regulates acid base balance.
ACID

BASE IMBALANCES
Buffer systems
Acute and chronic metabolic acidosis
Acute and chronic metabolic alkalosis
Acute and chronic respiratory acidosis
Acute and chronic respiratory alkalosis
Blood Gas Analysis

Types of Intravenous Solution

Hypotonic
Hypertonic
Isotonic
Edema
Capillary acid
Carbon dioxide dissolved in plasma
Regulation of Acid Base
Buffers
Carbonic Acid
Carbonic dioxide dissolved in plasma.
Serum bicarbonate (HCO3)
Major extracellular buffer in the blood.
KIDNEY regulate its generation and excretion.
Arterial Blood Gas Analysis
Normal Values
pH = 7.35 3.45
pCO2 = 35 45 mmHg
HCO3 = 22 26 mEq/L
Steps in ABG Analysis
1. Determine the pH
a. Low = ACIDIC
b. High = ALKALOSIS
2. Determine the area affected
a. Lungs = RESPIRATORY
b. Kidneys = METABOLIC
3. Determine the level of compensation
a. Uncompensated
b. Partially compensated

12

c. Fully compensated

RESPIRATORY

pH

pCO2

Acidosis
Alkalosis

METABOLIC

pH

HCO3

Acidosis
Alkalosis

HCO3
COMPENSATED

UNCOMPENSATED

N or
N or
pCO2

COMPENSATED

UNCOMPENSATED

N or
N or

13