Fluid and electrolyte and acid base balance

Fluids and Electrolytes

Body is 60% fluids

ICF=40%       

ECF=20% (Intravascular=5%; Interstitial=15%)

Solvent – the medium (usually water) that contains some particles.

Solutes – particles that are dissolved in solvent :salts, sugars, amino acids.

Electrolytes

•Chemical compounds in solution that have the ability to conduct an electrical current

Break into charged particles called ions

•Positively charged CATIONS

•Negatively charges : ANIONS

FUNCTIONS OF ELECTROLYTES

•Promote neuromuscular irritability

•Maintain body fluid volume and osmolality

•Distribute body water between fluid compartments

Function of Body Water

ECF

•Maintains blood volume

•Transport system to and from the cell

ICF

•Internal aqueous medium for cellular chemical function

MOVEMENTS OF FLUIDS BETWEEN COMPARTMENTS

•Diffusion

•Osmosis

•Active Transport

•Hydrostatic Pressure

•Colloid Osmotic Pressure

•Filtration

Types of solution

Crystalloids: Intravenous Fluids

1.Isotonic (equal osmolality with plasma)

   0.9% NaCL,Ringer’s Solution,Lactated Ringer’s, D5H20

2.Hypotonic (lower osmolality than plasma)

0.45% NaCL

3.Hypertonic (higher osmolality than plasma)

D5.9% NSS, D5.45% NSS, D10 H20,D5LR

Colloidal Solution

Aminosol 5%

Dextran 40

              INTRAVENOUS THERAPY

Purpose:

1.Maintenance of fluid & electrolyte balance

2.Replacement of fluid & electrolyte loss

3.Provision of nutrients

4.Provision of a route for medications

Average Fluid Intake

1.         Drink = 1,500ml/day.

2.         Food = 800 ml/day.

3.            Oxidation = 300 ml/day.

Average Fluid Loss

1.         Urine = 1,500 ml/day.

2.         Lung = 400 ml/day.

3.         Skin = 600 ml/day.

4.         Feces = 100ml/day.

Fluid Volume Deficit

An imbalance in fluid volume in which there is loss of fluid from the body not compensated for by an adequate intake of water.

•Excess Water Loss = FLUID VOLUME DEFICIT

Example: Simple Dehydration : water and electrolytes are lost in the same proportion

. Assessment

•Dry mucous   membranes

•Concentrated urine, ↓urine output

•Thready,↑PR,↑RR

•Orthostatic hypotension

•↓ BP

•Flat neck veins

•↓ CVP

•Diminished  peripheral pulse

•Dry skin

 Implementation

• fluid replacement

• weigh client daily

• monitor intake and output

• monitor urine specific gravity

Fluid Volume Excess

•           fluid intake or fluid retention exceeds the body’s fluid needs.

•           Also called overhydration or fluid overload

•           Excess Water Intake/Retention = FLUID VOLUME EXCESS

           

Example : Overhydration

1. Assessment

•Lethargy

•Confusion

•Muscle cramps

•Diarrhea

•Delirium

•Weakness

•Seizure

•Rapid PR

•↑Urinary output

•Nausea and vomiting

Nursing Interventions:

•Monitor vital signs, daily weight, and hemodynamic status.

•Monitor I & O.

•Monitor electrolyte levels & body system status.

•Prevent further fluid overload then restore normal fluid balance.

•Administer prescribed diuretics.

•  Report warning signs of hypervolemia.

SODIUM

Normal Value : 135-145 mEq/L

Common Food Sources : table salt, soy sauce, cured meats, dairy products (milk, cheese, butter), ketchup, canned food, snack food (chips, crackers). Note: instant oatmeal has salt.

Hyponatremia

 sodium level below 135 mEq/L

Causes:

1.            Increased sodium excretion.

2.            Inadequate sodium intake.

3.Dilution of serum sodium 

Assessment

•Nausea & vomiting

•Lethargy

•Confusion

•Muscle cramps

•Diarrhea

•Delirium

•Weakness

•Seizure

•Rapid PR

•↑Urinary output

Implementation

•Assess neurological status.

•Monitor electrolyte results and I & O accurately

•Administer IV fluids

•Increase oral sodium intake.

•Maintain seizure precautions.

•If hypovolemia: IV saline fluids; If hypervolemia: diuretics.

•If taking Lithium, monitor lithium levels because hyponatremia can cause decrease in lithium excretion and result in toxicity.

B. Hypernatremia  - sodium level exceeding 145 mEq/L

Causes:

1.            Decreased sodium excretion – corticosteroids, renal failure, Cushings Synd.

2.            Increased sodium intake – excess ingestion or IV fluids with sodium.

3.            Decreased water intake – NPO, Low fluid intake.

4.            Increased water loss – fever, diaphoresis.

Symptoms

           decreased contractility and output of heart

-            hypervolemia : pulmonary edema

-            spontaneous muscle twitching later weakness.

-           ** Altered mental/ cerebral functioning is the most common manifestation.

-            Increased urine specific gravity, decreased urine output.

Implementation

•Gradual replacement of water (in excess of sodium)

•ADH replacement, vasopressin administration (for patients with diabetes insipidus)

•Medications:

•Diuretics

•Diet therapy

•↓ Na+

           

POTASSIUM

Normal value = 3.5 – 5.1 mEq/L

Common food sources: avocado, raisins, pork, beef, cantaloupe, spinach, bananas, fish, oranges, strawberries, mushrooms, carrots, potatoes, tomatoes.

** Potassium is the major cation of the intracellular fluid. Small changes in extracellular potassium concentrations are very significant.

A. Hypokalemia

 - level below 3.5 mEq/L

Causes

1.            Potassium Loss – use of meds such as diuretics, Conns Synd (increase in aldosterone), vomiting, diarrhea.

2.            Inadequate intake

3.            Intracellular shift – alkalosis, hyperinsulinism, TPN feedings.

4.         Dilution of serum potassium – water intoxication, IV fluids with low K.

Assessment

•          Thready, weak pulse

•          Cardiac arrhythmias, ECG : ST depression

•          Shallow respiration

•          Anxiety, lethargy, confusion

•          Muscle weakness

•          Decreased GI motility, nausea, vomiting. 

•          Decreased urine specific gravity, increased output.

Implementation

•monitor ECG

•Oral or IV potassium

•Fluids to increase urinary output

•IV fluids

B. Hyperkalemia

- level exceeding 5.1 mEq/L

Causes

1.         Excess intake – overingestion of foods or meds, rapid infusion.

2.            Decreased excretion – potassium-sparing diurectics, renal failure.

3.            Extracellular shift – tissue damage, acidosis, vigorouse drawing of blood destroying RBC’s

Assessment

•           irregular heart rate, dysrhythmias; slow, weak pulse, decreased BP

•           ECG : tall T waves, widened QRS complexes, prolonged PR interval.

•           Skeletal muscle weakness, may lead to respiratory failure.

•           Early: muscle twitching, cramps, paresthesias.

•           Late: profound muscle weakness, paralysis.

•           Increased GI motility, diarrhea.

Implementation

•          monitor VS, affected systems, place on cardiac monitor.

•          Discontinue IV potassium or oral potassium supplements.

•          Restrict K in diet.

•          K excreting diuretics.

•          IV  glucose with insulin to move excess K into cells.

CALCIUM

Normal levels : 8.6 to 10.0 mg/dl

Plays an important role in excitable tissues : heart, muscle, nerves.

Common food sources : yogurt, milk, rhubarb, collard greens, cheese, tofu, spinach, broccoli, green beans, carrots

A. Hypocalcemia

- level below 8.6 mg/dl

Causes

1.            Inadequate absorption – low oral intake, lactose intolerance, malabsorption syndromes such as Crohns disease, celiac sprue, low intake of vit. D, ESRD.

2.            Increased excretion – renal failure, diarrhea, wound drainage.

3.            Conditions that decrese serum levels – alkalosis, medications, acute pancreatitis, **hyperphosphatemia, disease or removal of parathyroid glands.

Assessment

•          Decrease heart rate and contractility

•          Hypotension, diminished pulses.

•          Irritable skeletal muscles: twitching, cramps

•          Hyperactive deep tendon reflexes.

•          +Trousseau’s and Chvostek’s sign.

  

Implementation

• monitor VS and systems affected.

•Oral calcium or IV supplements

•Meds that increase calcium : aluminum hydroxide reduces phosphorus causing increase in calcium; vitamin D aids in absorption.

•Quiet environment, seizure precautions.

B. Hypercalcemia

 - level beyond 10 mg/dl.

Causes

1.            Increased absorption – excess oral intake of calcium or vit.D.

2.            Decreased excretion – renal failure, thiazide diuretics.

3.            Increased bone resorption – malignancy, immobility, hyperparathyroid/thyroid

4.            Hemoconcentration – dehydration

Assessment

•     Increased heart rate early but   bradycardia in late stage.

•           Increased BP, bounding pulses

•           Weak respiration, muscle weakness

•           Disorientation, lethargy, coma.

•           Formation of renal calculi

•           Decreased GI motility, anorexia, nausea.

Implementation

-           monitor VS, systems affected, cardiac monitor.

-            Discontinue oral or IV solutions with calcium, vit. D

-           IV normal saline to restore balance

-           Severe: dialysis

 •  

MAGNESIUM

Normal value: 1.6 – 2.6 mg/dl

Common food sources: green leafy vegetables, avocado, white tuna, milk, yogurt, oats

-           As calcium goes, so does magnesium. Hypocalcemia frequently accompanies hypomagnesemia, so signs are similar and interventions also aim to restore normal serum calcium level.

-            Monitor for reduced deep tendon reflexes when administering magnesium since reduced DTR’s suggest hypermagnesemia.

PHOSPHORUS

Normal value: 2.7 – 4.5 mg/dl

Common food sources: fish, pork, beef, chicken, organ meats, nuts.

   A decrease in phosphorus is accompanied by increase in calcium. Inverse relationship. Problems that occur in hyperphosphatemia center on the hypocalcemia that results when serum phosphorus levels increase. 

Acid – is a proton donor (HCL, Sulfuric,phosphoric ,carbonic acids

            A strong acid is the one that highly dissociate and produces a high concentration   

            Of hydrogen ions

Base – a hydrogen ion acceptor.They bind free hydrogen ions,reducing their concentration

Buffer – a substance that reduces the change in free hydrogen ion concentration of a solution on the addition of an acid or base

Acid Base Balance

The body has two main defense mechanisms against too much acid:

(There are other mechanisms but these are the important ones.

1. Respiratory

- if too much H2CO3 is produced by the above reactions, the lungs can remove it in the form of CO2.

- inability to remove CO2 due to hypoventilation causes acidosis.

- removal of too much CO2 by hyperventilation causes alkalosis.

2. Metabolic

- the kidneys can supply (recover) additional buffer base HCO3 to compensate for acidosis.

 - inability of the kidneys to recover HCO3 causes acidosis.

Drawing Arterial Blood Gases

1.         Obtain vital signs.

2.            Determine if arterial line is in place so arterial puncture is not necessary.

3.         Do Allen Test for determining patency of collateral circulation

a.         Apply direct pressure over the clients ulnar and radial arteries simultaneously.

b.         While pressure is applied, ask the client to open and close the hand repeatedly; the hand should blanch.

c.         Release pressure from the ulnar artery while compressing the radial artery and assess the color of the extremity distal to the pressure point.

d.         If pinkness fails to return within 6 seconds, the ulnar artery is insufficient, indicating that the radial artery should not be used for obtaining a blood specimen.

4.         Draw into heparinized syringe.

5.         Must be sterile.

6.         Discard if in contact with room air.

7.         Keep on ice, transport to lab immediately.

8.         Apply pressure to puncture site for 5 to 10 minutes.

9.         On the lab form always record the clients temperature and any oxygen being received.

Analyzing Arterial Blood Gases

Normal Values

pH: 7.35-7.45

PCO2: 35-45 mmHg

HCO3: 22-27 mEq/L

PO2: 80-100 mmHg

step 1 - examine pH

if low, indicates acidosis --
if high, indicates alkalosis --
if normal, check to see if borderline (may be compensation)

step 2 - examine CO2

if high, indicates respiratory acidosis (with low pH)
if low, indicates respiratory alkalosis (with high pH)
if normal, check for compensatory problem

step 3 - examine HCO3

üif high, indicates metabolic alkalosis (with high pH)
if low, indicates metabolic acidosis (with low pH)
if normal, check for compensatory condition

step 4 - check PO2 levels

üif low, indicates an interference with ventilation process (should evaluate the patient)
if normal, indicates patient is getting enough oxygen

step 5 - check signs/symptoms of patient

üThis analysis is for the patient whose respiratory status is fairly stable clinically, but acid/base balance is questionable. Following is a step-by-step account of how to analyze ABG if the prime concern is oxygenation.

pH 7.51, pCO2 40, HCO3- 31:

            a.            Normal

            b.            Uncompensated metabolic alkalosis

            c.            compensated respiratory acidosis

            d.            Uncompensated respiratory alkalosis

pH 7.33, pCO2 29, HCO3- 16:

            a.            Uncompensated respiratory alkalosis

            b.            Uncompensated metabolic acidosis

            c.            Compensated respiratory acidosis

            d.            Uncompensated metabolic acidosis

           

pH 7.40, pCO2 40, HCO3- 24:

            a.            Normal

            b.            Uncompensated metabolic acidosis

            c.            Compensated respiratory acidosis

            d.            Compensated metabolic acidosis

pH 7.12, pCO2 60, HCO3- 29:

            a.            Uncompensated metabolic acidosis

            b.            Uncompensated respiratory acidosis

            c.            Compensated respiratory acidosis

            d.            Compensated metabolic acidosis

pH 7.48, pCO2 30, HCO3- 23:

            a.            Uncompensated metabolic alkalosis

            b.            Uncompensated respiratory alkalosis

            c.            Compensated respiratory alkalosis

            d.            Compensated metabolic alkalosis

pH 7.62, pCO2 47, HCO3- 30:     

            a.            Uncompensated metabolic alkalosis

            b.            Uncompensated respiratory alkalosis

            c. compensated respiratory alkalosis

            d. compensated metabolic alkalosis