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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 ¾
 Contains fluids that surrounds the cells
 e.g. Lymph

b. Intravascular ¼
 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 the normal body
 Maintains ICF. 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  EFC:


Ions. MAJOR CATIONS: Sodium
MAJOR ANIONS: Chloride
 Positively charged ions: CATIONS.
 IFC:
 Negatively charged ions: ANIONS. MAJOR CATIONS: Potassium
MAJOR ANIONS: Phosphate

 FUNCTION OF ELECTROLYTES
 Promote neuromuscular irritability.
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 Maintain body fluid volume and osmolarity.
 Distribute water between fluid compartments.
 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 Output
 Water in food = 1,000 mls  Skin = 500 mls
 Water from oxidation = 300 mls  Lungs = 300 mls
 Water as liquid = 1,200 mls  Feces = 150 mls
 Kidneys = 1,500 mls
TOTAL : 2,500 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

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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.

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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.
 Ca absorption in GIT
s. Ca.  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  Excessive sweating


 Third – space fluid shift (edema and effusion)  Fever
 Electrolyte and acid – base imbalances  Hemorrhage
 Abdominal surgery  Nasogastric drainage
 Diabetes Mellitus  Renal failure with increased urination
 Excessive diuretic therapy  BUN will be elevated due to low volume
 Excessive laxative use (Normal BUN = 10 -25)
 Vomiting and diarrhea

Signs and symptoms

a. Increased heart rate d. Delayed capillary refill


b. Orthostatic hypotension e. Cool, Pale skin
c. Restlessness / Anxiety

Danger Signs

a. Deterioration in mental status e. Orthostatic hypotension progressing to mark


b. Thirst hypotension
c. Tachycardia f. Urine output drops below 10 mL / hr.
d. Delayed capillary refill g. Cool, Pale skin over the arms and legs

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h. Weight loss k. Weak or absent peripheral pulses
i. Flat jugular veins l. Shock
j. Decreased central venous pressure

Diagnostic test

1. Normal or high serum sodium > 145 mEq/L 3. Elevated creatinine and BUN ratio
2. Hemorrhage – decreased hemoglobin and 4. Increase urine specific gravity
hematocrit 5. Increased serum osmolality

Medical Management

1. IV fluids replacement
2. Blood transfusion
3. Vasopressors such as dopamine
4. Oxygen therapy
5. Surgery

Nursing Intervention

1. Monitor I and O frequently. 10. Bleeding – apply direct continuous pressure to


2. Normal urinary output = 30 – 60 cc / hr. the area and elevate it.
3. Check O2 sats and draw blood gases. 11. Monitor patient’s mental status and vital signs.
4. Auscultate lungs (side to side). 12. Monitor quality of peripheral pulses and skin
5. Check temperature distal from heart. temperature.
6. Give a fluid bolus as ordered. 13. Encourage to drink fluid appropriately.
7. Ensure patient airway. 14. Weigh patient daily to monitor the progress of
8. Apply oxygen as ordered. treatment.
9. Lower the head of the bed to show a declining 15. Provide effective skin care to prevent skin
blood pressure. 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  Nephrotic syndrome


Blood or plasma replacement  Corticosteriod therapy
 High intake of dietary sodium  Hyperaldosteronism
 Heart failure  Low intake of dietary protein
 Renal failure  Remobilization of fluids after burn treatment
 Cirrhosis of the liver  Consumption of excessive amount of sodium

Signs and symptoms

a. Increased cardiac output f. Increased weight


b. Rapid and bounding pulse g. Increased urine output
c. Crackles h. Shortness of breath and wheezing
d. Tachycardia i. Distended neck veins
e. Increase BP , pulse pressure and CVP j. Edema

Diagnostic Findings

a. Low hematocrit
b. Low serum potassium and BUN levels
c. Decreased serum osmolality
d. Low O2 level
e. Pulmonary congestion through X - ray

Medical Management

1. Restriction of fluid and sodium intake 5. O2 and bed rest


2. Diuretic 6. Hemodialysis / continuous renal replacement
3. Morphine and nitroglycerine therapy (CRRT)
4. Digoxin

Nursing Intervention

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1. Assess patient’s vital signs and hemodynamic 6. Follow ABG result and watch for a drop in O2
status. level or changes in acid – base balance.
2. Monitor for respiratory patterns for worsening 7. Raise the head of the bed.
distress. 8. Restrict fluid intake.
3. Watch for distended veins in hands and neck. 9. Maintain IV access for administration of
4. Record intake and output hourly. medications.
5. Listen to breath sounds regularly to assess for 10. Weigh the patient daily.
pulmonary edema. 11. Offer emotional support.

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 • Table salts
• Cheese • Salty snacks foods
• Ketchup • Seafoods
• Processed meats

HYPONATREMIA
 Sodium loss or water excess

Etiology

 Treatment with diuretics  “Trapping” of sodium and water


 Restricted sodium intake  Edema, ascites, burns or small bowel obstruction
 Loss from GI or biliary drainage and draining  Diaphoresis – warm climate, exercise, fever, and
fistulas “salt – wasting nephritis”
 Decreased aldosterone secretion (Addison’s
disease)

Sign and symptoms ( ECF,  ICF)

a. Headache f. Abdominal cramps


b. Muscle weakness g. Weight loss
c. Fatigue and apathy h. Feelings of apprehension
d. Postural hypotension i. Seizures and coma
e. Anorexia, nausea and vomiting

Collaborative Management

1. Treatment of shock
2. Replace other electrolytes depleted (K, Ca, HCO3)
3. Salt, salty foods in diet
4. 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  Rapid infusion of saline or IV
hyperventilation and diarrhea.  Water deprivation
 High Sodium intake
 Salt tablets  Na   ECF osmolality  ICF moves into ECF 
ICF dehydration

Signs and symptoms

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a. Extreme thirst f. Tachycardia
b. Dry, sticky mucous membrane g. Fatigue
c. Oliguria h. Restlessness
d. Firm, rubbery tissue turgor, excitement, i. Disorientation
agitation j. Hallucination
e. Red, dry, swollen tongue

Collaborative Management

1. Monitor I and O.
2. Restrict sodium in diet.
3. Monitor behavioral changes.
4. Increase oral fluids or D5W / IV.
5. Diuretics
6. 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

INCREASED LOSS SHIFT OF POTASSIUM INTO CELLS


DECREASED INTAKE
 Aldosterone (No change in total body
 Food and fluids as in potassium)
Gastrointestinal losses
starvation. Treatment of diabetic acidosis
Potassium �losing diuretics
Failure to replace losses. Metabolic alkalosis
Loss from cells as in trauma, burns

HYPOKALEMIA

CV
MUSCLE KIDNEY
GIT
CNS Decreased in
Weakness Anorexia
standing BP
Anorexia   Capacity
Lethargy Dysrhythmias
Nausea and Flaccid paralysis concentration
Diminished 
vomiting Weakness of waste
deep tendon ECG changes
Abdominial respiratory muscles 
reflexes 
distention  Water loss
Confusion Myocardial
 Respiratory arrest 
Mental damage
Paralytic ileus (Probably cause of Thirst
depression 
death in 
Cardiac Arrest
hypokalemia) Kidney Damage

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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 DECREASED LOSS SHIFT OF POTASSIUM OUT


Dietary intake in excess of Potassium – sparing OF CELLS
kidney’s ability to excrete. Diuretics Extensive trauma
Excess parenteral Renal failure Crushing injuries
administration. Adrenal insuffiency Metabolic acidosis

HYPERKALEMIA

MUSCLES CV
CNS KIDNEY
GIT
(Early) Conduction
Numbness Irritability disturbance Oliguria
Nausea and
(Late)
vomiting
Tingling Weakness Ventricular
sensation fibrillation 
Diarrhea Colic

Flaccid Cardiac Arrest Anuria
Paralysis

Collaborative Management

1. Avoid Potassium – rich foods. 4. Polysterone sulfonate (exchange resin


2. Promote bedrest. kayexalate).
3. 10 % glucose with regular insulin / IV. 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.  Vitamin D and PTH increases GI calcium
 Equal concentrations in ICF and ECF. absorption.
 Maintain cell membranes shape. Calcitonin = Blood to bone
 Acts as an enzyme activator within the Parathyroid hormone = Bone to blood.
cells.
 Aids coagulation. Dietary Sources
• Yogurt, low fat
 Two types: • Milk
a. Ionized • Rhubarb
b. Plasma protein bound • Collard green
• Cheese
 Free ionized calcium is needed for: • Tofu
a. Blood coagulation • Spinach
b. Smooth, skeletal and cardiac muscle • Broccoli
function • Green beans
c. Nerve function • Carrots
d. Bone and teeth formation
HYPOCALCEMIA DECREASED GI TRACT AND
DECREASED IONIZED INADEQUATE BONE ABSORPTION
EXCESS LOSS  Vitamin D
CALCIUM INTAKE
Large transfusion with  PTH
Kidney disease Decreased dietary
citrated blood  Magnesium
Draining fistula intake
alkalosis  Calcitonin
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HYPOCALCEMIA

GI TRACT CV
BONES CNS MUSCLES
OTHER
Increased Dysrhymias
Osteoporosis Tingling Muscle Spasm
Abnormal Peristalsis
deposits of  
  
calcium body Nausea and
tissue Vomiting Cardiac Arrest
Fracture Convulsion Tetany
Diarrhea

 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. High calcium diet 5. Vitamin D, PTH supplement


2. Calcium gluconate 6. Phosphate – binder (AL – OH)
3. Oral calcium salts   Phosphate   Calcium
4. Monitor breathing (laryngeal stridor) 7. Safety precaution (seizures may occur).

HYPERCALCEMIA

LOSS FROM BONES INCREASE IN FACTORS CAUSING


EXCESS INTAKE
Immobilization MOBILIZATION FROM BONE
 Calcium diet (especially
Carcinoma with bone  Parathyroid hormone
milk)
Metastases  Vitamin D and steroid
Antacid containing calcium.
Multiple myeloma therapy

HYPERCALCEMIA

MUSCLES
KIDNEY CNS CV
BONES
Muscles fatigue,
Stones  Deep tendon Hypotonia Depressed activity
Bone pain
reflexes  

  Dysrhythmias
Osteoporosis
Lethargy  Gastrointestinal 

Kidney  Tract
Fracture
Damage Coma 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.

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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 • Peas
broccoli • Potatoes
• Avocado • Pork, Beef and Chicken
• Canned white tuna fish • Raisins
• Low fat yogurt • Peanut butter
• Cooked rolled oats • Cauliflower
• Milk

HYPOMAGNESEMIA (Tetany)

  s magnesium   neuromuscular irritability by acetycholine realease   sensitivity of the myoneural


junction.
  Calcium   Magnesium ;  Calcium   Magnesium
 Hypomagnesemia potentiates action of digitalis

IMPAIRED ABSORPTION FROM GI TRACT


Malabsorption syndromes EXCESSIVE EXCRETION
DECREASE INTAKE
Alcohol withdrawal syndrome Aldosterone
Prolonged malnutrition
Hypercalcemia Condition causing large
Starvation
Diarrhea losses of urine
Draining gastrointestinal fistulas

HYPOMAGNESEMIA

MENTAL CNS CV
CHANGES MUSCLES

Convulsion Tachycardia
Agitation Cramps
Paresthesias Hypotension
Depression Spasticity
Tremor Dysrhythmias
Tetany
Confusion Ataxia

Collaborative Management

1. Dietary supplement : Fruit, green vegetables, whole grains, cereal, milk, meat, nuts, and seafoods.
2. Magnesium sulfate oral / parenteral.
3. Promote safety, prevention from injury.
4. Monitor for laryngeal stridor.
5. 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


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Signs and symptoms

a. Decreased BP
b. Thirst, nausea and vomiting
c. Drowsiness
d. Loss of DTR’s (deep tendon reflexes)

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  Use of antacid / sucralfate


tracellular fluid.  Inadequate Vitamin D.
 Decrease in intestinal absorption of phosphorus.  Chronic diarrhea and laxative abuse.
 Increase loss of phosphorus through kidneys.  Decrease dietary intake.
 Respiratory alkalosis  Increase PTH.
 Insulin – transports glucose and phosphorus into the
cells.

Signs and Symptoms

a. Muscle weakness f. Myalgia


b. Diplopia g. Respiratory failure
c. Malaise and anorexia h. Paresthesia
d. Weakened hand grasp i. Memory loss
e. Slurred speech / dysphagia j. Seizures / coma

Medical Management

1. Phosphorus replacement
2. High phosphorus diet
3. Neura – Phos and Neura – Phos – K
4. IV phosphorus replacement

Nursing Management

1. Monitor for sign and symptoms of this 4. Monitor rate and depth of respirations.
imbalance. 5. Monitor for signs of heart failure.
2. Monitor vital signs. 6. Ensure client maintains bed rest.
3. Assess the patient’s level of consciousness and 7. Record intake and output.
neurologic status.

HYPERPHOSPHATEMIA
 Occurs when serum phosphorus level exceed 2.6 mEq/L.

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Risk Factors

 Impaired renal excretion of phosphorus.  Shift of phosphorus from intracellular fluid to


 Increase dietary intake of phosphorus. extracellular fluid.

Signs and Symptoms

a. Hypocalcemia d. Hyperreflexia
b. Paresthesia e. (+) chvostek’s test and trousseau’s sign.
c. Muscle spasm 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
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2. Determine the area affected
a. Lungs = RESPIRATORY
b. Kidneys = METABOLIC

3. Determine the level of compensation


a. Uncompensated
b. Partially compensated
c. Fully compensated

HCO3
RESPIRATORY pH pCO2
COMPENSATED UNCOMPENSATED
Acidosis    N or 
Alkalosis    N or 

pCO2
METABOLIC pH HCO3
COMPENSATED UNCOMPENSATED
Acidosis    N or 
Alkalosis    N or 

13