Funda Fluids Elect.
Funda Fluids Elect.
Funda Fluids Elect.
Osmolarity
Another term that describes the concentration of solutions that is
measured in milliosmoles per liter (mOsm/L).
Tonicity- is the ability of all the solutes to cause an osmotic driving force
that promotes water movement from one compartment to another; the
control of tonicity determines the normal state of cellular hydration and cell
size.
Osmotic Pressure - is the amount of hydrostatic pressure needed to stop the
flow of water by osmosis; it is primarily determined by the concentration of
solutes.
Oncotic Pressure - is the osmotic pressure exerted by proteins (eg, albumin)
III. ELECTROLYTES:
A. Salts or minerals in the extracellular or intracellular body fluids.
B. If positively charged – CATIONS (Na, K, Ca, Mg, H ions); if negatively
charged – ANIONS (Chloride, Bicarbonate, Phosphate, Sulfate, Proteinate ions)
C. Common Electrolytes and normal blood values:
Magnesium (Mg) 1.3 to 2.1 mEq/L
This is arranged 1,2,3,4 for
Phosphorus 2.5 to 4.6 mEq/L
easy recall
Potassium (K) 3.5 to 5.5 mEq/L
Keep in mind that the only
Calcium (Ca) 4.5 to 5.3 mEq/L
high value is sodium
Sodium (Na) 135 to 148 mEq/L
A.Potassium (K)
Major ICF electrolyte; 98% of K are inside the cell
Constantly moving in and out of cell under the sodium- PISO – Potassium
potassium pump In, Sodium Out
Regulated by kidneys
Important in neuromuscular function
Influences skeletal and cardiac muscle activity (hypoKalemia : muscle
weakness/spasm; hyperKalemia: standstill of the heart)
Alterations in its concentration change myocardial irritability and rhythm
Kidneys are primary regulators of K balance; 80% is excreted daily from
body
Sources include banana, whole grains, meat, legumes, fruits and vegetables
B. Sodium (Na)
Most abundant electrolyte in the ECF (primary regulator of ECF volume)
Major regulator of body fluids (edematous: lower sodium intake)
Controls water distribution throughout the body
A gain or loss of Na = a gain or loss of water
Establish electrochemical state responsible for muscle contraction and
transmission of nerve impulses
Sodium is regulated by salt intake, aldosterone, and urinary output
Sources include table salt, processed meats, snacks and canned food
C. Calcium
99% of calcium located in skeletal system
Essential for cell membrane integrity, cardiac contraction, healthy bones and
teeth, and functioning of nerves and muscles
Plays a major role in transmitting nerve impulses and helps regulate muscle
contraction & relaxation including heart muscles. (hypocalcemia: Chvostek
sign and carpopedal spasm)
Instrumental in activating enzymes that stimulate chemical reactions in the
body
Calcium is , phosphorus
D. Magnesium
Next to K, abundant in the ICF, a Cation
Activator of many ICF enzymes – plays a role in CHO & CHON
metabolism
Important in neuromuscular function – acts directly on the myoneural
junction’ affects muscular irritability and contractility (excess – diminishes;
deficit – increases)
Produces sedative effect at neuromuscular junction (inhibiting release of
acetylcholine)
Exerts effects on CV system, acting peripherally to produce vasodilation
(thought to have direct effect on peripheral arteries and arterioles)
relaxed the muscles
causes extra movements i.e. tremors, etc.= irritable
Cardiovascular system = vasodilation in peripherals
Hypermagnesemia: below 30 ml/hr, below 12 bpm, and loss of dtr
E. Phosphorus
Primary anion of the ICF
Critical constituent of all body tissues, assists in structure of genetic material
Critical to nerve, muscle, RBC formation
Participates in cellular energy metabolism (CHO, CHON, Fats)
Combines with calcium to provide structural support to bones and teeth
Essential to formation of adenosine triphosphate (ATP)
F. Chloride
Major anion of the ECF; found more in interstitial & lymph fluid than in
blood
Contained in gastric & pancreatic juices & in sweat
Sodium & Chloride in water make up the composition of the ECF & assist
in determining osmotic pressure
Serum level of Chloride reflects a change in dilution or concentration of the
ECF & does so in direct proportion to sodium
Aldosterone ↑ sodium reabsorption thereby ↑ chloride reabsorption
The choroid plexus where CSF forms depends on sodium & chloride to
attract water to form the fluid portion of the CSF
Has an inverse relationship with bicarbonates (as chloride moves from
plasma to RBCs, bicarbonates moves back into the plasma)
V. FLUID REGULATION:
A. OSMORECEPTOR SYSTEM
B. CIRCULATORY SYSTEM
C. THIRST CENTER
Located in hypothalamus
Stimulated by
B. PARATHYROID
HYPERNATREMIA
Causes:
Excessive water losses
Decrease water intake
Excessive sodium intake
Manifestations:
Dry and sticky mucous membrane
Thirst
Rough dry tongue
Fever
Restlessness
Weakness
Disorientation
Treatment:
Fluid replacement
Treat the underlying cause
HYPOKALEMIA
Causes:
Inadequate intake
Excessive renal losses
Excessive gastrointestinal losses
Manifestations:
Anorexia
Abdominal distention
Paralytic Ileus
Muscle weakness
Dysrhythmias
ECG changes
Prolongation of PR interval
Depressed ST segment
Prominent U wave
Treatment:
Increase intake of foods high in
potassium content ( meats, dried
fruits, orange juice, bananas)
Potassium supplement
(oral/parenteral)
HYPERKALEMIA
Causes:
Excessive intake
Release from intracellular compartment
Inadequate elimination by kidneys
Manifestations:
Diarrhea
Colic
Nausea
Irritability
Muscle weakness
ECG changes
Low P wave
Prolongation of PR interval
Widening of QRS complex
Peaked T wave
Vomiting
Weakness
Muscle cramps **BQ**
Risk of CARDIAC ARREST
Treatment:
Decrease potassium intake
Increase potassium output
Infusion of insulin and glucose
HYPOCALCEMIA
Causes:
Impaired ability to mobilize calcium from the bones
Decrease intake or absorption
Abnormal renal losses
Increased protein binding or
chelation
Increased sequestration
Manifestations:
Abdominal and muscle cramps
Stridor
Tetany
Neuromuscular irritability
Tingling sensation
ECG changes
Ventricular fibrillation
Heart block
Widened QT interval
Hypotension
Fracture
Osteomalacia
Bone pain
Cardiac insufficiency
Treatment:
Infusion of calcium containing solution
Calcium gluconate
Calcium gluceptate
Calcium chloride
Oral intake of calcium (1glass = 300mg)
Vitamin D administration
HYPERCALCEMIA
Causes:
Increased intestinal absorption
Increased bone resorption
Decreased elimination
Manifestations:
Impaired ability to concentrate urine and exposure of kidney to increased
calcium concentration
Deep bone pain
Flank pain
Muscle weakness
Depressed deep tendon reflexes
Constipation
Nausea and vomiting
Confusion
Impaired memory
Anorexia
Hypertension
Lethargy
Personality and behavioral changes
Stupor and coma
ECG changes
Shortening of the QT interval
AV block
Treatment:
Directed towards rehydration and measures to increase urinary excretion of
calcium and inhibit release of calcium from the bone.
Fluid replacement
Diuretics and Sodium chloride administration
Calcitonin
Biphosphonates (fosamax, actonel) – prmotes osteoblastic activity of bone
(bone formation)
HYPOPHOSPHATEMIA
Causes:
Impaired renal function – most common
Decreased intestinal absorption
Increased renal elimination
Malnutrition and intracellular shifts
Manifestations:
Deep bone pain
Seizures
Flank pain
Muscle weakness
Tremors
Ataxia
Paresthesias
Anemia
Platelet dysfunction
Impaired WBC function
Joint stiffness
Treatment:
Replacement therapy (1 glass of milk = 250mg)
Oral or parenteral preparation
CONTRAINDICATED: Renal problem/Hypercalcemia
HYPERPHOSPHATEMIA
Causes:
Acute phosphate overload
Intracellular-to-extracellular shifts
Impaired Elimination
Manifestations:
Tetany
Muscle spasms
Tingling of fingers and around the mouth
Lethargy
Hyporeflexia
Confusion
Coma
Hypotension
Cardiac dysrhythmias
Cardiac arrest
Treatment:
Directed at the cause of the disorder
Dietary restriction
Calcium based Phosphate binders ex. Basaljel, amphogel
Dialysis
HYPOMAGNESEMIA
Causes:
Impaired intake or absorption
Increase losses
Manifestations:
Dysphagia
Muscle cramps
Neuromuscular irritability
Hyperreflexia
Dysrhythmias
Vertigo
Personality change
Tetany
Hypertension
Tachycardia
Treatment:
Magnesium replacement
HYPERMAGNESEMIA
Causes:
Excessive intake
Decreased excretion
Manifestations:
Facial flushing
Nausea and vomiting
Depressed deep tendon reflex
Respiratory depression
Cardiac arrest
Lethargy
Confusion
Coma
Hypotension
Oliguria
Treatment:
Cessation of Magnesium administration
Calcium administration
Peritoneal Dialysis/Hemodialysis
HYPOCHLOREMIA
Causes:
Chloride-deficient formulas
Salt-restricted diets
GI tube drainage
Severe vomiting and diarrhea
Manifestations:
Hyperexcitability of muscles
Tetany
Hyperactive deep tendon reflexes
Weakness
Twitching
Muscle cramps
Treatment:
Normal saline (0.9% sodium chloride) or half-strength saline (0.45% sodium
chloride) solution is administered IV to replace the chloride
The physician may reevaluate whether patients receiving diuretics (loop,
osmotic, or thiazide) should discontinue these medications or change to
another diuretic
Foods high in chloride are provided; these include tomato juice, salty broth,
canned vegetables, processed meats, and fruits.
A patient who drinks free water (water without electrolytes) or bottled water
will excrete large amounts of chloride; therefore, this kind of water should
be avoided.
RESPIRATORY ALKALOSIS
A clinical condition in which the arterial pH is greater than 7.45 and the PaCO2
is less than 38 mm Hg
Respiratory alkalosis is always due to hyperventilation, which causes excessive
“blowing off” of CO2 and, hence, a decrease in the plasma carbonic acid
concentration.
Causes:
Extreme anxiety
Hypoxemia
Early phase of salicylate intoxication
Gram-negative bacteremia
Inappropriate ventilator settings that do not match the patient’s requirements
Manifestations:
ABG changes
Constriction of cerebral vessels
Cardiac dysrhythmias
Dizziness
Seizures
Treatment:
Treatment is directed in removing ingested toxins or by treating fever,
sepsis, or CNS infections.
In SEVERE respiratory alkalosis, the patient may need to breathe slowly or
breathe into a paper bag.
Sedation and Tranquilizers
Nursing Diagnoses:
Anxiety related to cause of respiratory alkalosis.
Impaired gas exchange related to alveolar hyperventilation.
Ineffective breathing pattern related to deep, rapid breathing
Nursing Interventions:
Provide supportive care for the underlying cause of respiratory alkalosis as
ordered.
Stay with the patient during periods of extreme stress and anxiety. Offer
reassurance and maintain a calm, quite environment.
Help patient identify factors that precipitate anxiety and help him find
coping mechanisms/ activities.
RESPIRATORY ACIDOSIS
A clinical disorder in which the pH is less than 7.35 and the PaCO2 is greater
than 42 mm Hg.
Respiratory acidosis is always due to inadequate excretion of CO2 with
inadequate ventilation, resulting in elevated plasma CO2 levels and thus
elevated carbonic acid (H2CO3) levels
In addition to an elevated PaCO2, hypoventilation usually causes a decrease in
PaO2.
Causes:
Acute pulmonary edema
Aspiration of a foreign object
Atelectasis
Pneumothorax
Overdose of sedatives
Sleep apnea syndrome
Administration of oxygen to a patient with chronic hypercapnia (excessive
CO2 in the blood)
Severe pneumonia
Acute respiratory distress syndrome.
Respiratory acidosis can also occur in diseases that impair respiratory
muscles, such as muscular dystrophy, myasthenia gravis, and Guillain-Barré
syndrome.
Manifestations:
ABG changes
Dilation of cerebral vessels
Headache
Weakness
Behavioral changes
Coma
Acid urine
Skin warm and flushed
Paralysis
Shock
Cardiac Arrest
Treatment: Directed to correct the source of alveolar hypoventilation.
Mechanical Ventilation
Administration of Sodium Bicarbonate (pH of less than 7.15)
Nursing Diagnoses:
Fear related to threat of death.
Impaired gas exchange related to alveolar hypoventilation.
Ineffective breathing pattern related to rapid shallow respirations.
Nursing Interventions:
Be prepared to treat or remove the underlying cause.
Maintain adequate hydration by administering IV fluids.
Give oxygen if partial pressure of arterial oxygen drops.
Start mechanical ventilation if hypoventilation cannot be corrected
immediately.
Perform tracheal suctioning regularly and chest physiotherapy, if ordered.
METABOLIC ACIDOSIS
Manifestations:
ABG changes
Confusion
Hyperactive reflexes
Tetany
Convulsions
Hypotension
Dysrhythmias
Respiratory acidosis
Decreased rate and depth of respiration
Increased urine pH
Treatment:
Mild Metabolic Alkalosis may require NO treatment.
Severe Metabolic Alkalosis includes administration of IV Ammonium
Chloride, Potassium chloride and normal saline solutions (replace gastric
losses)
Oral or IV Acetazolamide (enhances renal bicarbonate/ potassium excretion)
Nursing Diagnoses:
Disturbed thought processes related to neurologic dysfunction.
Decreased cardiac output related to AV arrhythmias.
Risk for injury related to tetany
Nursing Interventions:
When administering IV solutions containing potassium salts, dilute
potassium with the prescribed IV solution and use an IV infusion pump.
Infuse ammonium chloride 0.9% IV no faster than 1L over 4 hours; Faster
administration may cause RBC hemolysis. Don’t give ammonium chloride
to patients with hepatic/ renal disease.
Observe seizure precautions, and provide a safe environment for the patient
with altered thought process. Orient the patient as needed.
Irrigate the patient’s NG tube with normal saline solution instead of plain
water to prevent loss of gastric electrolytes.
X. SHOCK
Is an acute, life-threatening condition in which body tissues are inadequately
perfused or unable to utilize oxygen.
Types of Shock:
Hypovolemic - state characterized by inadequate amounts of blood volume in
the intravascular space.
Cardiogenic – a condition in which myocardial damage renders the heart unable
to pump enough blood to maintain adequate perfusion .
Obstructive – occurs when blood flow is impeded by a mechanical or physical
obstruction.
Distributive – refers to conditions involving alterations in the distribution of
intravascular volume.
Neurogenic – severe pain
Anaphylactic – systemic allergy
Septic – systemic infection
Stages of Shock:
Compensated / non-progressive - Vital organs remain adequately perfused
because of compensatory mechanism
Decompensated / progressive - Vital organs become underperfused and
compensatory mechanisms become ineffective, resulting in systemic
manifestations.
Irreversible - The extent of shock is so severe that therapeutic interventions
become useless; death eventually occurs
Collaborative Management:
Assess the primary cause of shock in cases of third-space shifting to prevent
further volume loss.
Assess hemodynamic status and all major body systems.
Monitor intake and output.
Monitor CVP. 4-12 cm water
Monitor vital signs. Bp up, rr and pr low
Maintain airway and provide cardiac and pulmonary support.
Institute fluid replacement therapy as ordered.
Administer steroids, as ordered depending on the causative injury.
Analgesics: Morphine Sulfate
Antihistamines
Administer blood transfusion as indicated.
Institute management for specific cause
Provide supportive care as indicated.
A. Types of IV Solutions:
ISOTONIC
Fluids that are classified as isotonic have a total
osmolality close to that of the ECF and do not
cause red blood cells to shrink or swell
Examples:
D5W
A solution of D5W has a serum
osmolality of 252 mOsm/L
Once administered, the glucose is
rapidly metabolized, and this initially
isotonic solution then disperses as a
hypotonic fluid, one-third extracellular and two-thirds intracellular.
It is essential to consider this action of D5W, especially if the
patient is at risk for increased intracranial pressure.
During fluid resuscitation, this solution should not be used because
it can cause hyperglycemia.
Therefore, D5W is used mainly to supply water and to correct an
increased serum osmolality.
About 1 L of D5W provides fewer than 200 kcal and is a minor
source of calories for the body’s daily requirements.
D. Drip Chambers
1. Microdrip System – delivers 60 drops/ml & is used when small volumes are being
delivered (ex. less than 50 to 70ml/min); this reduces the risk of clotting the IV line due
to slow infusion rates.
2. Macrodrip System – delivers 10, 15, 20 drops/ml & is used to deliver solution in large
quantities & fast rates
E. Calculations
1. Flow Rate
Drops per minute = total volume infused x drop factor (drops/ml)
total time for infusion in minutes
Example: Infuse 150ml of PNSS in 1 hour using a macrodrip set (15 drops/ml)
Drops per minute = 150 ml x 15 drops/ml
60 minutes
= 2250drops divided by 60 minutes
= 37.5 or 38 drops/minute
G. Changing Schedules
1. Intravenous solution containers are changed only when a small amount of fluid
remains in the neck of the container & fluid still remains in the drip chamber.
2. All IV bags should be changed every 24 hours regardless of how much solution
remains.
3. Tubings should be changed every 48 hours to decrease the incidence of phlebitis &
infection but some studies indicate 72-hr interval may be appropriate.
4. The dressing over the IV site is changed according to hospital protocol – generally
every 48-72 hours.
H. Monitoring An IV Infusion
1. Observe the rate of flow every hour
If the rate is too fast, slow it so that the infusion will be completed at the planned
time
If the rate is too slow, check agency practice. Some agencies permits adjustment of
rate of flow 3ml/min or less; 3ml/min or more may require DR’s order
If the rate of flow is 150ml/hour or more, check the rate more frequently (ex. q15 or
30 minutes)
2. Inspect the patency of the IV tubing
Inspect the tubing for pinches or kinks or obstruction to flow
Open the drip regulator & observe for a rapid flow of fluid from the solution
container into the drip chamber
Lower the solution container below the level of infusion site & observe for a return
of blood from the vein
Observe the position of the solution container. If it is less than 1 meter above the
IV site, readjust it to the correct height of the pole
Observe the drip chamber. If it is less than half full, squeeze the chamber to allow
the correct amount of fluid to flow in
If there is a leakage, locate the source.
3. Inspect the insertion site for fluid infiltration
Palpate the surrounding tissue for edema
Feel the surrounding skin for changes in temperature
4. If infiltration is not evident but the infusion is not flowing, determine whether the
needle is dislodged from the vein
5. Inspect insertion site for phlebitis
6. Inspect the intravenous site for bleeding
7. Patient teaching to maintain infusion system:
Call for assistance if the solution stops dripping or the site becomes swollen
Avoid sudden twisting or turning movements of the arm with the needle or catheter
Avoid stretching or placing tension on the tubing
Try to keep the tubing from dangling below the level of the needle
Notify nurse if:
- there is sudden change in flow rate or if the solution stops dripping
- the solution container is nearly empty
- there is blood in the IV tubing
- discomfort or swelling is experienced at the IV site
I. Intravenous Push
Aka IV bolus; refers to the administration of a medication from a syringe & needle
directly into an ongoing IV infusion. It may also be given directly into a vein or
heparin lock
Indications:
1. For emergency administration of cardiopulmonary resuscitative procedures,
allowing rapid concentration of a medication in the pt’s bloodstream when quicker
response to the medication is required
2. To administer “loading” doses of a drug that will be continued via infusion
3. To reduce the pt discomfort by limiting the need for IM injections
4. To avoid incompatibility problems that may occur when several medication are
mixed in one bottle
5. To deliver drugs to pts unable to take them by mouth (coma) or IM (coagulation
disorder)
Precautions:
1. Dilute the drug as indicated by pharmacy references. Many medications are quite
irritating to the veins, requiring sufficient dilution
2. Most medications are given slowly (rarely over less than one minute); sometimes as
long as 30 minutes are required.
3. If IV push is to be given with an ongoing IV infusion or to follow another IV push
medication, flush the tubing or cannula with saline prior to & following
administration of drug
J. Heparin Lock
An intermittent infusion reservoir that permits administration of periodic intravenous
medications without fluid administration & aspiration of blood samples for lab analysis
After IV cannulation, attach the heparin lock cap; flush with 0.5ml of heparin solution
All IV medications given via heparin locks are administered utilizing the “SASH”
method: S–aline flush A-dminister meds S–aline flush H-eparin flush
K. IV Piggyback
Administering medication via the fluid pathway of an established primary infusion line
Features & Advantages:
1. Drugs may be given on an intermittent basis through a “keep open” infusion
2. The secondary bottle contains the medications; this maybe single or multiple dose
3. When desired, the primary infusion is clamped off & the prescribed amount of
medication from the secondary bottle is administered; or 2 solutions may run
simultaneously depending on the tubing design
4. When a check valve is present, it performs the ff functions:
a. Permits the primary infusion to flow after the medication has been administered
b. Prevents air from entering the system
c. Prevents secondary fluid from “running dry”
d. Permits less mixing of primary fluid with secondary solution
5. Higher flow rates can be achieved by elevating either of the receptacle.