FLUIDS AND ELECTROLYTES

I. BASIC PRINCIPLES ABOUT BODY FLUIDS:

A. Water constitutes over 50 to 60% of individual’s weight. (Female: 50%; Male:
60%)
B. Factors affecting amount of fluid: age (the younger the more fluids), gender
(male has more fluids), body fat (lean has more fluids)
C. Located in 2 compartments:
a. Intracellular (within the cell; 2/3)
b. Extracellular (outside the cell; 1/3)
i. Intravascular (inside the blood vessels),
ii. Interstitial (fluids that surrounds the cell, ex Lymphs)
iii. Transcellular (cerebrospinal, pericardial, synovial, intraocular,
pleural, sweat, digestive secretions)
D. Fluids in these 2 compartments shift to one another in order to maintain
equilibrium (balance) between two spaces.
E. Fluid losses can disturb the equilibrium (dehydration, burns, hemorrhage)
F. Third spacing or fluid shifts happens when fluids from intravascular space does
not got to intracellular space but goes elsewhere (urine output, heart rate;
BP, edema, body weight)

II. MOVEMENT OF FLUIDS AND ELECTROLYTES:

A. Diffusion: movement of particles from an area of greater concentration to an
area of lesser concentration; Examples: exchange of O2 & CO2 between the
pulmonary capillaries & alveoli; tendency of sodium to move from ECF
 compartment, where sodium concentration is high, to the ICF, where its
concentration is low.
B. Active Transport: movement across cell membranes requiring energy from an
outside source (Insulin transport for glucose delivery to the cell, Insulin also
carries potassium)
C. Osmosis: movement of water through a semipermeable membrane (from lesser
concentration to an area of greater concentration)
D. Other Important Terms:
 Osmolality
 The concentration of fluid that affects the movement of water between
fluid compartments by osmosis
 Measures the solute concentration per kilogram in blood and urine
 Also a measure of a solution’s ability to create osmotic pressure and
affect the movement of water
 Serum osmolality primarily reflects the concentration of sodium
 Urine osmolality is determined by urea, creatinine, and uric acid
 When measured with serum osmolality, urine osmolality is the most
reliable indicator of urine concentration
 Osmolality is reported as milliosmoles per kilogram of water
(mOsm/kg).
 Normal serum osmolality is 280 to 300 mOsm/kg, and normal urine
osmolality is 250 to 900 mOsm/kg.

 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

IV. SIGNIFICANCE OF THE ELECTROLYTES:

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)

Signs and Symptoms of Fluid and Electrolyte Imbalances

DEFICIT EXCESS
Volume Acute weight loss (> 5%), drop in body Acute weight gain (> 5%),
temperature, dry skin and mucous edema, hypertension, distended
membranes, postural hypotension, neck veins, dyspnea, rales
longitudinal wrinkles or furrows of tongue,
oliguria or anuria
Sodium Abdominal cramps, apprehension, Dry, sticky mucous
convulsions, fingerprinting on sternum, membranes, flushed skin,
oliguria or anuria oliguria or anuria, thirst, rough
and dry tongue
Potassium Anorexia, abdominal distention, intestinal Diarrhea, intestinal colic,
ileus, muscle weakness, tenderness, and irritability, nausea,
cramps parasthesias; flaccid paralysis,
cardiac arrhythmias and arrest
Calcium Abdominal cramps, positive Chovstek's and Anorexia, nausea, vomiting,
Trousseau's signs, tingling of extremities, abdominal pain and distention,
tetany mental confusion
BicarbonateDeep, rapid breathing (Kussmaul), shortness Depressed respirations, muscle
of breath on exertion, stupor, weakness hypertonicity, tetany (metabolic
(metabolic acidosis) alkalosis)
Magnesium Positive Chovstek's sign, seizures, Hypotension, flushing,
disorientation, hyperactive deep tendon lethargy, dysarthria, hypoactive
reflexes, tremor deep tendon reflexes,
respiratory depression

V. FLUID REGULATION:

A. OSMORECEPTOR SYSTEM

 Balances fluid intake volume by the regulation of water output volume

 Dehydration stimulates osmoreceptors which activate the thirst control center;
person feels thirsty and seeks water
 Also stimulates antidiuretic hormone (ADH) secretion which decreases
urinary output by causing the reabsorption of water in the tubules

B. CIRCULATORY SYSTEM

 Increases in fluid intake increase circulatory volume

 This increased volume stimulates the kidney for an increased glomerular
filtration rate
 End result is an increase in urine output to decrease the initial circulatory
volume

C. THIRST CENTER

 Located in hypothalamus
 Stimulated by

 Increased plasma osmolality

 Angiotensin II
 Dry pharyngeal mucous membranes
 Decreased plasma volume
 Depleted potassium
 Psychological factors
VI. MAINTENANCE OF ELECTROLYTE BALANCE

A. ALDOSTERONE - HORMONE (MINERALCORTICOID)

 When extracellular fluid sodium decreases or potassium levels increase

adrenal cortex secretes aldosterone
 Kidneys stimulated by aldosterone to increase reabsorption of sodium and
decreased reabsorption of potassium
 Results in water reabsorption and increased blood volume

B. PARATHYROID

 Parathyroid secretes parathyroid hormone (PTH), also called parathormone

 Stimulates release of calcium from bone, reabsorption in small intestine and
kidney tubules
 When serum calcium level is low, PTH secretion increases
 When serum calcium level rises, PTH secretion falls
 High levels of active vitamin D inhibit PTH and low levels or magnesium
stimulate PTH secretion

VII. FLUID & ELECTROLYTE IMBALANCES

 FLUID VOLUME DEFICIT

 A decrease in extracellular fluid, including circulating blood volume
 Causes:
 Inadequate fluid intake
 Excessive GI fluid losses
 Excessive renal losses
 Excessive skin losses
 Third-space losses
 Manifestations:
 Acute weight loss
 Decrease skin turgor
 Dry mucous membrane
 Oliguria
 Increased Hematocrit and BUN
 Hypothermia
 Treatment:
 Fluid replacement (isotonic electrolyte)
 Treat underlying cause

 FLUID VOLUME EXCESS

 An increase in the extracellular fluid compartment

 Causes:
 Inadequate sodium/ water elimination
 Excessive sodium intake in relation to output
 Excessive fluid intake in relation to output
 Manifestations:
 Acute weight gain
 Edema
 Crackles
 Shortness of breath
 Decreased Hematocrit and BUN
 Distended neck vein
 Hypertension
 Strong and bounding pulse
 Treatment Goal: Provide balance between sodium and water intake and output.
 Na restricted diet
 Diuretic therapy – commonly used
 HYPONATREMIA
 Causes:
 Excessive Na losses and replacement with tap water or sodium-free solution
 Excessive water intake in relation to output
 Manifestations:
 Nausea
 Malaise
 Lethargy
 Headache
 Abdominal Cramps
 Apprehension
 Seizures
 Treatment:
 If due to H2O intoxication – Limit intake
 Na deficiency – Saline solution infusion
 Symptomatic HypoNa – Hypertonic Saline solution and Diuretics
 Treat the underlying cause

 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.

 HYPERCHLOREMIA inverse relationship with bicarbonate

 Cause: Loss of bicarbonate ions via the kidney or the GI tract with a
corresponding increase in chloride ions
 Manifestations:
 Tachypnea
 Weakness
 Lethargy
 Deep, rapid respirations
 Diminished cognitive ability
 Hypertension
 If untreated, hyperchloremia can lead to a decrease in cardiac output,
dysrhythmias and coma
 A high chloride level is accompanied by a high sodium level and fluid
retention
 Treatment: Correcting the underlying cause of hyperchloremia and restoring
electrolyte, fluid, and acid–base balance are essential:
 Lactated Ringer’s solution may be prescribed to convert lactate to
bicarbonate in the liver, which will increase the base bicarbonate level and
correct the acidosis.
 Sodium bicarbonate may be given IV to increase bicarbonate levels, which
leads to the renal excretion of chloride ions as bicarbonate and chloride
compete for combination with sodium.
 Diuretics may be administered to eliminate chloride as well.
 Sodium, fluids, and chloride are restricted.
VIII. MAINTENANCE OF ACID-BASE BALANCE

 Plasma pH is an indicator of hydrogen ion (H+) concentration

 The H+ concentration is extremely important: the greater the concentration, the
more acidic the solution and the lower the pH. The lower the H+ concentration,
the more alkaline the solution and the higher the pH.
 The pH range compatible with life (6.8–7.8) represents a tenfold difference in
H+ concentration in plasma.
 Homeostatic mechanisms keep pH within a normal range (7.35–7.45). These
mechanisms consist of the following:
 BUFFER SYSTEMS
 Prevent major changes in the pH of body fluids by removing or
releasing H+
 Act quickly to prevent excessive changes in H+ concentration
 Hydrogen ions are buffered by both intracellular and extracellular
buffers
 The body’s major extracellular buffer system is the bicarbonate-
carbonic acid buffer system.
 This is the system that is assessed when arterial blood gases are
measured.
 Normally, there are 20 parts of bicarbonate (HCO3−) to one part of
carbonic acid (H2CO3). If this ratio is altered, the pH will change.
 It is the ratio of HCO3− to H2CO3 that is important in maintaining
pH, not absolute values.
 Carbon dioxide (CO2) is a potential acid; when dissolved in water, it
becomes carbonic acid (CO2 + H2O = H2CO3).
 Thus, when CO2 is increased, the carbonic acid content is also
increased, and vice versa.
  If either bicarbonate or carbonic acid is increased or decreased so that
the 20:1 ratio is no longer maintained, acid–base imbalance results.
 KIDNEYS
 The kidneys regulate the bicarbonate level in the ECF
 It can regenerate bicarbonate ions as well as reabsorb them from the
renal tubular cells.
 In respiratory acidosis and most cases of metabolic acidosis, the
kidneys excrete hydrogen ions and conserve bicarbonate ions to help
restore balance.
 In respiratory and metabolic alkalosis, the kidneys retain hydrogen
ions and excrete bicarbonate ions to help restore balance.
 The kidneys obviously cannot compensate for the metabolic acidosis
created by renal failure. Renal compensation for imbalances is
relatively slow (a matter of hours or days).
 LUNGS
 The lungs, under the control of the medulla, control the CO2 and thus
the carbonic acid content of the ECF
 It does so by adjusting ventilation in response to the amount of CO2 in
the blood.
 A rise in the partial pressure of CO2 in arterial blood (PaCO2) is a
powerful stimulant to respiration.
 Of course, the partial pressure of oxygen in arterial blood (PaO2) also
influences respiration. Its effect, however, is not as marked as that
produced by the PaCO2.
 In metabolic acidosis, the respiratory rate increases, causing greater
elimination of CO2 (to reduce the acid load).
 In metabolic alkalosis, the respiratory rate decreases, causing CO2 to
be retained (to increase the acid load).

IX. ACID-BASE IMBALANCES:

 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

 Metabolic acidosis is a clinical disturbance characterized by a low pH

(increased H+ concentration) and a low plasma bicarbonate concentration
 Causes:
 Diarrhea
 Lower intestinal fistulas
 Ureterostomies
 Use of diuretics; early renal insufficiency
 Excessive administration of chloride
 Hypoaldosteronism
 Excessive burning of fats
 Manifestations:
 ABG changes
 Anorexia
 Nausea and vomiting
 Abdominal pain
 Weakness
 Lethargy
 General malaise
 Confusion
 Stupor
 Coma
 Depression of vital functions
 Peripheral vasodilation
 Bradycardia
 Cardiac dysrhythmias
 Acid urine
 Kussmaul’s Breathing
 Hyperkalemia
 Increased ammonia in urine
 Treatment:
 Acute Metabolic Acidosis, treatment may include IV administration of
Sodium Bicarbonate.
 Chronic Metabolic Acidosis, treatment may include oral bicarbonate.
 Others:
 Treat the underlying cause
 Mechanical ventilation
 Nursing Interventions:
 Provide care to eliminate the underlying cause of metabolic acidosis.
 Administer sodium bicarbonate.
 Position the patient to promote chest expansion and turn him every 2 hours.
 Orient the patient frequently.
 METABOLIC ALKALOSIS

 A clinical disturbance characterized by a high pH (decreased H+ concentration)

and a high plasma bicarbonate concentration.
 Causes:
 Vomiting or gastric suction with loss of hydrogen and chloride ions
 Pyloric stenosis, in which only gastric fluid is lost; gastric fluid has an acid
pH (usually 1–3)
 Loss of potassium, such as diuretic therapy that promotes excretion of
potassium (eg, thiazides, furosemide)
 Excessive adrenocorticoid hormones (as in hyperaldosteronism and
Cushing’s syndrome)
 Excessive alkali ingestion from antacids containing bicarbonate or from
using sodium bicarbonate during cardiopulmonary resuscitation

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

 Physiologic Responses to Shock

 Vasoconstriction
 A compensatory mechanism
 SNS activation
 Adrenal medulla - epinephrine and norepinephrine
 Adrenal cortex - glucocorticoids and mineralocorticoids
 Tachycardia
 Tachypnea
 Skin color and temperature changes
 Early stages: Blood is shunted to the brain and heart and away from the
skin and other organs that tolerate ischemia well  skin feels cool and
pale.
 Hypotension: when compensatory mechanisms fail
 Coagulation abnormalities
 Metabolic waste products and microaggregates of platelets and clotting
factors accumulate in the capillary bed, resulting on clotting.
 Thrombocytopenia may occur in septic shock
 Hyperglycemia
 In response to release of epinephrine, glycogen is broken down into
glucose
 Fluid shifts
 Activation of the RAAS (Renin-Angiotensin Aldosterone System)
 End organ damage: - due to tissue ischemia
 Impaired removal of waste products secondary to decreased renal
function. Destruction of liver and kidneys
 Hepatic dysfunction
 GI problems
 Kidney problems
 Nutritional deficits
 CNS Damage

 Signs and Symptoms of Shock:

 Early Stage
 Face – pale or cyanotic in color
 Skin – cold and clammy
 Breathing – irregular
 Pulse – rapid and weak
 Nausea and vomiting
  Weakness
 Thirsty
 Late Stage
 Apathetic or unresponsive
 Eyes – sunken with vacant expression
 Pupils are dilated
 Mottled skin appearance
 Low blood pressure
 Unconsciousness
 Body temperature falls

 First Aid and Preventive Management for Shock

 Proper Position tredelenburg
 Keep the victim lying down flat. (Safe position)
 Elevate the lower part of the body or foot or so. (Improves blood circulation)
 Place victim on his back with head and shoulder raised. (When there is
difficulty of breathing.)
 Keep victim on his/her side opposite his/her injury (Recovery, position). For
nauseated or vomiting victim.
 Proper Body Heat
 Maintain body temperature (must not be perspiring nor chilling).

 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.

XI. PARENTERAL FLUID THERAPY

 Also known as Intravenous (IV) Fluid Administration

 Purposes:
 To provide water, electrolytes, and nutrients to meet
daily requirements
 To replace water and correct electrolyte deficits
 To administer medications and blood products

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.

 Normal Saline Solution or PNSS, NSS, .9 NaCl

 Normal saline (0.9% sodium chloride) solution has a total
osmolality of 308 mOsm/L
 Because the osmolality is entirely contributed by electrolytes, the
solution remains within the ECF
 For this reason, normal saline solution is often used to correct an
extracellular volume deficit.
 Although referred to as “normal,” it contains only sodium and
chloride and does not actually simulate the ECF.
 It is used with administration of blood transfusions and to replace
large sodium losses, as in burn injuries.
 It is not used for heart failure, pulmonary edema, renal impairment,
or sodium retention.
 Normal saline does not supply calories.
 Lactated Ringer’s Solution
 Lactated Ringer’s solution contains potassium and calcium in
addition to sodium chloride
 It is used to correct dehydration and sodium depletion and replace
GI losses.
 Lactated Ringer’s solution contains bicarbonate precursors as well.
 HYPOTONIC .45NaCl, half-strength
 One purpose of hypotonic solutions is to replace cellular fluid, because it is
hypotonic as compared with plasma.
 SWELL
 Another is to provide free water for excretion of body wastes. At times,
hypotonic sodium solutions are used to treat hypernatremia and other
hyperosmolar conditions.
 Half-strength saline (0.45% sodium chloride) solution, with an osmolality of
154 mOsm/L, is frequently used. Multiple-electrolyte solutions are also
available.
 Excessive infusions of hypotonic solutions can lead to intravascular fluid
depletion, decreased blood pressure, cellular edema, and cell damage.
 HYPERTONIC – D5LR, D10W, TPN
 When normal saline solution or lactated Ringer’s solution contains 5%
dextrose, the total osmolality exceeds that of the ECF.
 SHRINK
 The dextrose is quickly metabolized, however, and only the isotonic
solution remains.
 Therefore, any effect on the intracellular compartment is temporary.
 Similarly, with hypotonic multiple-electrolyte solutions containing 5%
dextrose, once the dextrose is metabolized, these solutions disperse as
hypotonic fluids.
 Higher concentrations of dextrose, such as 50% dextrose in water, are
administered to help meet caloric requirements.
 These solutions are strongly hypertonic and must be administered into
central veins so that they can be diluted by rapid blood flow.
 Saline solutions are also available in osmolar concentrations greater than
that of the ECF.
 These solutions draw water from the ICF to the ECF and cause cells to
shrink. If administered rapidly or in large quantity, they may cause an
 extracellular volume excess and precipitate circulatory overload and
dehydration.
 As a result, these solutions must be administered cautiously and usually only
when the serum osmolality has decreased to dangerously low levels.

B. Criteria for Selecting a Vein Suitable for Venipuncture

1. Initial Considerations
 Use distal branches of large vein initially
 Select a vein that is easily palpated & feels soft
& full
 Locate a vein that is not crooked, scarred,
hardened or inflamed
2. Suitable Veins
 Back of the hand – metacarpal vein. Avoid
digital veins as possible
 The advantage of this site is that it permits
arm movement
 If later a vein problem develops at the site
another vein higher up the arm may be used
 Forearm – basilic or cephalic vein
 Inner aspect of the elbow, antecubital fossa,
median basilic, & median cephalic for relatively
short-term infusion
 These veins are large & easily accessible
 Note however, that this site precludes arm
movement
 Choose site below elbow crease for pt’s
comfort
 In adult patients, veins in lower extremities are
used as a last resort

C. Methods of Distending a Vein

1. Apply manual compression above site where cannula is to be inserted
2. Have the patient periodically clench his fist (if arm is used)
3. Massage area in direction of venous flow
4. Apply tourniquet at least 2-6 inches above planned insertion site fastening it with a slip
knot
5. Lightly tap vein site; this is done gently so that the vein is not injured
6. Allow extremity to be dependent (below the heart level) for a few minutes

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

2. Hourly Rate of Infusion

Milliliters per Hour = total infusion volume (ml)
total infusion time (hr)
Example: If 3liters is infused in 24 hours, how much is infused per hour?
First convert, liters into milliters (3x1000=3000ml)
Milliliters per Hour = 3000 ml
24hours
= 125ml/hr

3. Hours to Consume = Volume (ml)_______

Hourly rate infusion (ml/hr)
Example: 1 liter of D5W has been running for an hour. The flow rate is 125ml/hr.
How many hours will the infusion run before it is consumed?
1 liter = 1000 ml – 125 = 875 ml
Hours to Consume = 875ml divided by 125ml/hr = 7 hours

F. Factors Influencing Flow Rates

1. The position of the forearm – sometimes a change in the position of pt’s arm ↓ the
flow; slight pronation, supination, extension or elevation of the arm could ↑the flow
2. Flow is directly proportional to the height of the liquid column. Raising the height of
the infusion container may improve a sluggish flow.
3. Flow is directly proportional to the diameter of the tubing. The clamp on IV tubing
regulates the flow by changing the tubing diameter. In addition, the flow is faster
through large-gauge rather than small-gauge cannulas.
4. Flow is inversely proportional to the length of the tubing. Adding extension tubing to
an IV line will decrease the flow.
5. Flow is inversely proportional to the viscosity of a fluid. Viscous IV solutions, such as
blood, require a larger cannula than do water or saline solutions.

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.