Fluids and Electrolytes

Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

solute – the substance dissolved
solvent – substance in which the solute is dissolved
- usually water (universal solvent)
molar solution (M) - # of gram-molecular weights of solute
per liter of solution
osmolality – concentration of solute per kg of water
STI COLLEGE GLOBAL CITY normal range = 275-295 mOsm/kg of water
osmolarity – concentration of solute per L of solution
College of Nursing * since 1kg=1L, & water is the solvent of the human
body, osmolarity & osmolality are used interchangeably
MEDICAL AND SURGICAL NURSING

Fluids and Electrolytes
IV. Mechanisms of Body Fluid Movement (i.e. movement
Lecturer: Mark Fredderick R. Abejo RN, MAN of solutes, solvents across different extracellular
________________________________________________ locations)
A. Osmosis: water is mover; water moves from
FLUIDS & ELECTROLYTES lower concentration to higher concentration
1. Normal Osmolality of ICF and ECF:
I. Fluid Status of Human Body 275 – 295 mOsm/kg
A. Homeostasis: state of the body when 2. Types of solutions according to osmolality
maintaining a state of balance in the presence Isotonic: all solutions with osmolality
of constantly changing conditions same as that of plasma .Body cells placed
B. Includes balance of fluid, electrolytes, and acid- in isotonic fluid: neither shrink nor swell
base balance Hypertonic: fluid with greater
C. Body water intake and output approximately concentration of solutes than plasma
equal (2500 mL/24 hr.) Cells in hypertonic solution: water in
cells moves to outside to equalize
concentrations: cells will shrink
Adult body: 40L water, 60% body weight Hypotonic: fluid with lower concentration
2/3 intracellular of solutes than plasma Cells in hypotonic
1/3 extracellular (80% interstitial, 20% solution: water outside cells moves to
intravascular) inside of cells: cells will swell and
Infant: 70-80% water eventually burst (hemolyze)
Elderly: 40-50% water 3. Different intravenous solutions, used to
correct some abnormal conditions,
categorized according to osmolality:
II. Body Fluid Composition
A. Water: 60% of body weight B. Diffusion: solute molecules move from higher
B. Electrolytes: substances that become charged concentration to lower concentration
particles in solution 1. Solute, such as electrolytes, is the
1. Cations: positively charged (e.g. Na+, mover; not the water
K+) 2. Types: simple and facilitated
2. Anions: negatively charged (e.g. Cl-) (movement of large water-soluble
3. Both are measured in milliequivalents molecules)
per liter (mEq/L) C. Filtration: water and solutes move from area
C. Balance of hydrostatic pressure and osmotic of higher hydrostatic pressure to lower
pressure regulates movement of water hydrostatic pressure
between intravascular and interstitial spaces 1. Hydrostatic pressure is created by
pumping action of heart and gravity
III. Body Fluid Distribution: against capillary wall
A. 2 body compartments: 2. Usually occurs across capillary
1. Intracellular fluids (ICF): fluids membranes
within cells of body [major
intracellular electrolytes: Potassium D. Active Transport: molecules move across
(K+), Magnesium (Mg +2)] cell membranes against concentration
2. Extracellular fluids (ECF): fluid gradient; requires energy, e.g. Na – K pump
outside cells; [major extracellular
electrolytes: Sodium (Na+),
Chloride(Cl-)]; this is where
transportation of nutrients, oxygen,
and waste products occurs Hydrostatic pressure -pushes fluid out of vessels into tissue
space; higher to lower pressure
B. Locations of ECF: – due to water volume in vessels; greater in arterial end
1. Interstitial: fluid between most cells – swelling: varicose veins, fluid overload, kidney failure
2. Intravascular: fluid within blood & CHF
vessels; also called plasma Osmotic pressure -pulls fluid into vessels; from weaker
3. Transcellular: fluids of body concentration to stronger concentration
including urine, digestive secretion, - from plasma proteins; greater in venous end
cerebrospinal, pleural, synovial, - swelling: liver problems, nephrotic syndrome
intraocular, gonadal, pericardial

MS: Fluids and Electrolyte Abejo


V. Mechanisms that Regulate Homeostasis:
How the body adapts to fluid and electrolyte changes? ADH – produced by hypothalamus, released by posterior
pituitary when osmoreceptor or baroreceptor is
A. Thirst: primary regulator of water intake triggered in hypothalamus
(thirst center in brain)
B. Kidneys: regulator of volume and Aldosterone – produced by adrenal cortex; promotes Na &
osmolality by controlling excretion of water water reabsorption
and electrolytes
C. Renin-angiotension-aldosterone
mechanism: response to a drop in blood Sensible & Insensible Fluid Loss
pressure; results from vasoconstriction and
sodium regulation by aldosterone Sensible: urine, vomiting, suctioned secretions
D. Antidiuretic hormone: hormone to Insensible: lungs , skin, GI and evaporation
regulate water excretion; responds to
osmolality and blood volume
E. Atrial natriuretic factor: hormone from Normal Fluid Intake and Loss in Adults
atrial heart muscle in response to fluid
excess; causes increased urine output by Intake:
blocking aldosterone  Water in food 1,000 mls
 Water from oxidation 300 mls
Fluid Balance Regulation  Water in liquid 1,200 mls

Thirst reflex triggered by: TOTAL 2,500 mls
1. decreased salivation & dry mouth
2. increased osmotic pressure stimulates Output:
osmoreceptors in the hypothalamus  Skin 500 mls
3. decreased blood volume activates the  Lungs 300 mls
renin/angiontensin pathway, which simulates the  Feces 150 mls
thirst center in hypothalamus  Kidneys 1,500 mls
TOTAL 2,500 mls
Renin-Angiotensin
1. drop in blood volume in kidneys = renin released
2. renin = acts on plasma protein angiotensin
(released by the liver) to form angiotensin I
3. ACE = converts Angiotensin I to Angiotensin II in
the lungs
4. Angiotensin II = vasoconstriction & aldosterone
release


IV Fluids  Risk factors are the following:
Isotonic LR a. Diabetes Insipidus
PNSS (0.9%NSS) b. Adrenal insufficiency
NM c. Osmotic diuresis
d. Hemorrhage
Hypotonic D5W e. Coma
- isotonic in bag f. Third-spacing conditions like ascites,
- dextrose=quickly pancreatitis and burns
metabolized=hypotonic
D2.5W
0.45% NSS PATHOPHYSIOLOGY:
0.3% NSS
0.2% NSS Risk Factors --- inadequate fluids in the body ---- decreased
blood volume ----- decreased cellular hydration ---- cellular
Hypertonic D50W shrinkage ---- weight loss, decreased turgor, oliguria,
D10W
hypotension, weak pulse, etc.
D5NSS
D5LR
3%NSS
ASSESSMENT:

Colloids (usually CHONs) & Plasma expanders Physical examination
 Weight loss, tented skin turgor, dry mucus membrane
Dextran – synthetic polysaccharide, glucose solution  Hypotension
- increase concentration of blood, improving blood  Tachycardia
volume up to 24 hrs  Cool skin, acute weight loss
- contraindicated: heart failure, pulmonary edema,  Flat neck veins
cardiogenic shock, and renal failure  Decreased CVP

Hetastarch – like Dextran, but longer-acting Subjective cues
- expensive
- derived from corn starch  Thirst
 Nausea, anorexia
Composition of Fluids  Muscle weakness and cramps
 Change in mental state
Saline solutions – water, Na, Cl
Dextrose solutions – water or saline, calories
Lactated Ringer‟s – water, Na, Cl, K, Ca, lactate Laboratory findings
Plasma expanders – albumin, dextran, plasma protein 1. Elevated BUN due to depletion of fluids or decreased
(plasmanate) - increases oncotic pressure, pulling fluids renal perfusion
into circulation 2. Hemoconcentration
Parenteral hyperalimentation – fluid, electrolytes, amino 3. Possible Electrolyte imbalances: Hypokalemia,
acids, calories Hyperkalemia, Hyponatremia, hypernatremia
4. Urine specific gravity is increased (concentrated
A. FLUID VOLUME DEFICIT or HYPOVOLEMIA urine) above 1.020
 Definition: This is the loss of extra cellular fluid NURSING MANAGEMENT
volume that exceeds the intake of fluid. The loss of
water and electrolyte is in equal proportion. It can 1. Assess the ongoing status of the patient by doing an
be called in various terms- vascular, cellular or accurate input and output monitoring
intracellular dehydration. But the preferred term is 2. Monitor daily weights. Approximate weight loss 1
hypovolemia. kilogram = 1liter!
 Dehydration refers to loss of WATER alone, with 3. Monitor Vital signs, skin and tongue turgor, urinary
increased solutes concentration and sodium concentration, mental function and peripheral
concentration circulation
4. Prevent Fluid Volume Deficit from occurring by
Pathophysiology of Fluid Volume Deficit identifying risk patients and implement fluid
replacement therapy as needed promptly
 Etiologic conditions include: 5. Correct fluid Volume Deficit by offering fluids orally
a. Vomiting if tolerated, anti-emetics if with vomiting, and foods
b. Diarrhea with adequate electrolytes
c. Prolonged GI suctioning 6. Maintain skin integrity
d. Increased sweating 7. Provide frequent oral care
e. Inability to gain access to fluids 8. Teach patient to change position slowly to avoid
f. Inadequate fluid intake sudden postural hypotension
g. Massive third spacing



B. FLUID VOLUME EXCESS: HYPERVOLEMIA 4. Teach patient about edema, ascites, and fluid therapy.
 Definition : Refers to the isotonic expansion of Advise elevation of the extremities, restriction of
the ECF caused by the abnormal retention of fluids, necessity of paracentesis, dialysis and diuretic
water and sodium therapy.
 There is excessive retention of water and 5. Instruct patient to avoid over-the-counter medications
electrolytes in equal proportion. Serum sodium without first checking with the health care provider
concentration remains NORMAL because they may contain sodium

Pathophysiology of Fluid Volume Excess

 Etiologic conditions and Risks factors ELECTROLYTES
a. Congestive heart failure  Electrolytes are charged ions capable of conducting
b. Renal failure electricity and are solutes found in all body
c. Excessive fluid intake compartments.
d. Impaired ability to excrete fluid as in renal
disease Sources of electrolytes
e. Cirrhosis of the liver  Foods and ingested fluids, medications; IVF and
f. Consumption of excessive table salts TPN solutions
g. Administration of excessive IVF
h. Abnormal fluid retention Functions of Electrolytes
 Maintains fluid balance
 Regulates acid-base balance
PATHOPHYSIOLOGY  Needed for enzymatic secretion and activation
Excessive fluid --- expansion of blood volume ----- edema,  Needed for proper metabolism and effective
processes of muscular contraction, nerve
increased neck vein distention, tachycardia, hypertension. transmission
Types of Electrolytes
The Nursing Process in Fluid Volume Excess  CATIONS- positively charged ions; examples are
sodium, potassium, calcium
ASSESSMENT  ANIONS- negatively charged ions; examples are
Physical Examination chloride and phosphates]
 Increased weight gain  The major ICF cation is potassium (K+); the
 Increased urine output major ICF anion is Phosphates
 Moist crackles in the lungs  The major ECF cation is Sodium (Na+); the major
 Increased CVP ECF anion is Chloride (Cl-)
 Distended neck veins
 Wheezing
 Dependent edema
ELECTROLYTE IMBALANCES
Subjective cue/s
 Shortness of breath
 Change in mental state SODIUM

Laboratory findings  The most abundant cation in the ECF
1. BUN and Creatinine levels are LOW because of  Normal range in the blood is 135-145 mEq/L
dilution  A loss or gain of sodium is usually accompanied by a
2. Urine sodium and osmolality decreased (urine loss or gain of water.
becomes diluted)  Major contributor of the plasma Osmolality
3. CXR may show pulmonary congestion  Sources: Diet, medications, IVF. The minimum daily
requirement is 2 grams
IMPLEMENTATION Functions:
ASSIST IN MEDICAL INTERVENTION 1. Participates in the Na-K pump
1. Administer diuretics as prescribed 2. Assists in maintaining blood volume
2. Assist in hemodialysis 3. Assists in nerve transmission and muscle
3. Provide dietary restriction of sodium and water contraction
4. Primary determinant of ECF concentration.
NURSING MANAGEMENT
5. Controls water distribution throughout the body.
1. Continually assess the patient‟s condition by 6. Primary regulator of ECF volume.
measuring intake and output, daily weight monitoring,
7. Sodium also functions in the establishment of the
edema assessment and breath sounds
2. Prevent Fluid Volume Excess by adhering to diet electrochemical state necessary for muscle
prescription of low salt- foods. contraction and the transmission of nerve
3. Detect and Control Fluid Volume Excess by closely impulses.
monitoring IVF therapy, administering medications, 8. Regulations: skin, GIT, GUT, Aldosterone
providing rest periods, placing in semi-fowler‟s increases Na retention in the kidney
position for lung expansion and providing frequent
skin care for the edema



SODIUM DEFICIT: HYPONATREMIA In summary:

 Definition : Refers to a Sodium serum level of less Physical Examination
than 135 mEq/L. This may result from excessive  Altered mental status
sodium loss or excessive water gain.  Vomiting
 Lethargy
Pathophysiology  Muscle twitching and convulsions (if sodium level is
below 115 mEq/L)
Etiologic Factors  Focal weakness
a. Fluid loss such as from Vomiting and nasogastric
suctioning Subjective Cues
b. Diarrhea  Nausea
c. Sweating  Cramps
d. Use of diuretics  Anorexia
e. Fistula  Headache
Other factors Laboratory findings
a. Dilutional hyponatremia 1. Serum sodium level is less than 135 mEq/L
Water intoxication, compulsive water 2. Decreased serum osmolality
drinking where sodium level is diluted 3. Urine specific gravity is LOW if caused by sodium loss
with increased water intake 4. In SIADH, urine sodium is high and specific gravity is
b. SIADH HIGH
Excessive secretion of ADH causing
water retention and dilutional IMPLEMENTATION
hyponatremia
ASSIST IN MEDICAL INTERVENTION
1. Provide sodium replacement as ordered. Isotonic saline
PATHOPHYSIOLOGY is usually ordered.. Infuse the solution very cautiously.
Decrease sodium concentration --- hypotonicity of plasma -- The serum sodium must NOT be increased by greater
- water from the intravascular space will move out and go to than 12 mEq/L because of the danger of pontine
the intracellular compartment with a higher concentration --- osmotic demyelination
cell swelling --Water is pulled INTO the cell because of 2. Administer lithium and demeclocycline in SIADH
decreased extracellular sodium level and increased 3. Provide water restriction if with excess volume
intracellular concentration

NURSING MANAGEMENT
The Nursing Process in HYPONATREMIA
1. Provide continuous assessment by doing an accurate
ASSESSMENT intake and output, daily weights, mental status
Sodium Deficit (Hyponatremia) examination, urinary sodium levels and GI
manifestations. Maintain seizure precaution
Clinical Manifestations 2. Detect and control Hyponatremia by encouraging food
 Clinical manifestations of hyponatremia depend on the intake with high sodium content, monitoring patients
cause, magnitude, and rapidity of onset. on lithium therapy, monitoring input of fluids like IVF,
 Although nausea and abdominal cramping occur, most parenteral medication and feedings.
of the symptoms are neuropsychiatric and are probably 3. Return the Sodium level to Normal by restricting water
related to the cellular swelling and cerebral edema intake if the primary problem is water retention.
associated with hyponatremia. Administer sodium to normovolemic patient and
 As the extracellular sodium level decreases, the elevate the sodium slowly by using sodium chloride
cellular fluid becomes relatively more concentrated and solution
„pulls” water into the cells.
 In general, those patients having acute decline in serum
sodium levels have more severe symptoms and higher SODIUM EXCESS: HYPERNATREMIA
mortality rates than do those with more slowly
developing hyponatremia.  Serum Sodium level is higher than 145 mEq/L
 Features of hyponatremia associated with sodium loss  There is a gain of sodium in excess of water or a
and water gain include anorexia, muscle cramps, and a loss of water in excess of sodium.
feeling of exhaustion.
 When the serum sodium level drops below 115 mEq/L Pathophysiology:
(SI: 115 mmol/L), thee ff signs of increasing
intracranial pressure occurs: Etiologic factors
 lethargy a. Fluid deprivation
 Confusion b. Water loss from Watery diarrhea, fever, and
 muscular twitching hyperventilation
 focal weakness c. Administration of hypertonic solution
 hemiparesis d. Increased insensible water loss
 papilledema e. Inadequate water replacement, inability to swallow
 convulsions f. Seawater ingestion or excessive oral ingestion of salts



Other factors IMPLEMENTATION
a. Diabetes insipidus
ASSIST IN THE MEDICAL INTERVENTION
b. Heat stroke
c. Near drowning in ocean 1. Administer hypotonic electrolyte solution slowly as
d. Malfunction of dialysis ordered
2. Administer diuretics as ordered
Loop diuretics (thiazides ok)
PATHOPHYSIOLOGY 3. Desmopressin is prescribed for diabetes insipidus

Increased sodium concentration --- hypertonic plasma ---- NURSING MANAGEMENT
water will move out form the cell outside to the interstitial 1. Continuously monitor the patient by assessing
space ----- CELLULAR SHRINKAGE ----- then to the abnormal loses of water, noting for the thirst and
blood ---- Water pulled from cells because of increased elevated body temperature and behavioral changes
extracellular sodium level and decreased cellular fluid 2. Prevent hypernatremia by offering fluids regularly
concentration and plan with the physician alternative routes if oral
route is not possible. Ensure adequate water for
patients with DI. Administer IVF therapy cautiously
The Nursing Process in HYPERNATREMIA 3. Correct the Hypernatremia by monitoring the
patient‟s response to the IVF replacement. Administer
Sodium Excess (Hypernatremia) the hypotonic solution very slowly to prevent sudden
cerebral edema.
Clinical Manifestations 4. Monitor serum sodium level.
 primarily neurologic 5. Reposition client regularly, keep side-rails up, the bed
 Presumably the consequence of cellular dehydration. in low position and the call bell/light within reach.
 Hypernatremia results in a relatively concentrated ECF, 6. Provide teaching to avoid over-the counter
causing water to be pulled from the cells. medications without consultation as they may contain
 Clinically, these changes may be manifested by: sodium
o restlessness and weakness in moderate
hypernatremia
o disorientation, delusions, and
POTASSIUM
hallucinations in severe hypernatremia.
 Dehydration (hypernatremia) is often overlooked as the
primary reason for behavioral changes in the elderly.
 If hypernatremia is severe, permanent brain damage  The most abundant cation in the ICF
can occur (especially in children). Brain damage is  Potassium is the major intracellular electrolyte; in fact,
apparently due to subarachnoid hemorrhages that result 98% of the body‟s potassium is inside the cells.
from brain contraction.  The remaining 2% is in the ECF; it is this 2% that is
all-important in neuromuscular function.
A primary characteristic of hypernatremia is thirst.  Potassium is constantly moving in and out of cells
Thirst is so strong a defender of serum sodium levels in according to the body‟s needs, under the influence of
normal people that hypernatremia never occurs unless the the sodium-potassium pump.
person is unconscious or is denied access to water;  Normal range in the blood is 3.5-5 mEq/L
unfortunately, ill people may have an impaired thirst  Normal renal function is necessary for maintenance of
mechanism. Other signs include dry, swollen tongue and potassium balance, because 80-90% of the potassium is
sticky mucous membranes. A mild elevation in body excreted daily from the body by way of the kidneys.
temperature may occur, but on correction of the The other less than 20% is lost through the bowel and
hypernatremia the body temperature should return to sweat glands.
normal.  Major electrolyte maintaining ICF balance
 Sources- Diet, vegetables, fruits, IVF, medications
ASSESSMENT
Physical Examination Functions:
 Restlessness, elevated body temperature 1. Maintains ICF Osmolality
 Disorientation 2. Important for nerve conduction and muscle
 Dry, swollen tongue and sticky mucous membrane,
contraction
tented skin turgor
 Flushed skin, postural hypotension 3. Maintains acid-base balance
 Increased muscle tone and deep reflexes 4. Needed for metabolism of carbohydrates, fats and
 Peripheral and pulmonary edema proteins
5. Potassium influences both skeletal and cardiac muscle
Subjective Cues activity.
 Delusions and hallucinations ( For example, alterations in its concentration change
 Extreme thirst myocardial irritability and rhythm )
 Behavioral changes
6. Regulations: renal secretion and excretion,
Laboratory findings * Aldosterone promotes renal excretion
1. Serum sodium level exceeds 145 mEq/L * Acidosis promotes K exchange for hydrogen
2. Serum osmolality exceeds 295 mOsm/kg
3. Urine specific gravity and osmolality INCREASED
or elevated



POTASSIUM DEFICIT: HYPOKALEMIA

 Condition when the serum concentration of potassium
is less than 3.5 mEq/L

Pathophysiology

 Etiologic Factors
a. Gastro-intestinal loss of potassium such as
diarrhea and fistula
b. Vomiting and gastric suctioning
c. Metabolic alkalosis
d. Diaphoresis and renal disorders
e. Ileostomy

 Other factor/s
a. Hyperaldosteronism
b. Heart failure
c. Nephrotic syndrome
d. Use of potassium-losing diuretics
e. Insulin therapy
f. Starvation
g. Alcoholics and elderly

PATHOPHYSIOLOGY
IMPLEMENTATION
Decreased potassium in the body impaired nerve
excitation and transmission signs/symptoms such as ASSIST IN THE MEDICAL INTERVENTION
weakness, cardiac dysrhythmias etc.. 1. Provide oral or IV replacement of potassium
2. Infuse parenteral potassium supplement. Always dilute
the K in the IVF solution and administer with a pump.
The Nursing Process in Hypokalemia
IVF with potassium should be given no faster than 10-
20-mEq/ hour!
3. NEVER administer K by IV bolus or IM
Clinical Manifestations
 Potassium deficiency can result in widespread NURSING MANAGEMENT
derangements in physiologic functions and especially
nerve conduction. 1. Continuously monitor the patient by assessing the
 Most important, severe hypokalemia can result in death cardiac status, ECG monitoring, and digitalis
through cardiac or respiratory arrest. precaution
 Clinical signs rarely develop before the serum 2. Prevent hypokalemia by encouraging the patient to eat
potassium level has fallen below 3 mEq/L (51: 3 potassium rich foods like orange juice, bananas,
mmol/L) unless the rate of fall has been rapid. cantaloupe, peaches, potatoes, dates and apricots.
 Manifestations of hypokalemia include fatigue, 3. Correct hypokalemia by administering prescribed IV
anorexia, nausea, vomiting, muscle weakness, potassium replacement. The nurse must ensure that the
decreased bowel motility, paresthesias, dysrhythmias, kidney is functioning properly!
and increased sensitivity to digitalis. 4. Administer IV potassium no faster than 20 mEq/hour
 If prolonged, hypokalemia can lead to impaired renal and hook the patient on a cardiac monitor. To
concentrating ability, causing dilute urine, polyuria, EMPHASIZE: Potassium should NEVER be given IV
nocturia, and polydipsia bolus or IM!!
5. A concentration greater than 60 mEq/L is not advisable
ASSESSMENT for peripheral veins.
Physical examination
 Muscle weakness
 Decreased bowel motility and abdominal distention
 Paresthesias
POTASSIUM EXCESS: HYPERKALEMIA
 Dysrhythmias
 Increased sensitivity to digitalis  Serum potassium greater than 5.5 mEq/L
Pathophysiology
Subjective cues
 Nausea , anorexia and vomiting  Etiologic factors
 Fatigue, muscles cramps a. Iatrogenic, excessive intake of potassium
 Excessive thirst, if severe b. Renal failure- decreased renal excretion of
potassium
Laboratory findings c. Hypoaldosteronism and Addison‟s disease
1. Serum potassium is less than 3.5 mEq/L d. Improper use of potassium supplements
2. ECG: FLAT “T” waves, or inverted T waves,
depressed ST segment and presence of the “U” wave  Other factors
and prolonged PR interval. 1. Pseudohyperkalemia- tight tourniquet and
3. Metabolic alkalosis hemolysis of blood sample, marked leukocytosis


2. Transfusion of “old” banked blood
3. Acidosis
4. Severe tissue trauma

PATHOPHYSIOLOGY
Increased potassium in the body ---- Causing irritability of
the cardiac cells --- Possible arrhythmias!!

The Nursing Process in Hyperkalemia

Clinical Manifestations
 By far the most clinically important effect of
hyperkalemia is its effect on the myocardium.
 Cardiac effects of an elevated serum potassium level
are usually not significant below a concentration of 7
mEq/L (SI: 7 mmol/L), but they are almost always
present when the level is 8 mEq/L (SI: 8 mmol/L) or
greater.
 As the plasma potassium concentration is increased,
disturbances in cardiac conduction occur. IMPLEMENTATION
 The earliest changes, often occurring at a serum
potassium level greater than 6 mEq/ L (SI: 6 ASSIST IN MEDICAL INTERVENTION
mmol/L), are peaked narrow T waves and a shortened 1. Monitor the patient‟s cardiac status with cardiac
QT interval. machine
 If the serum potassium level continues to rise, the PR 2. Institute emergency therapy to lower potassium level
interval becomes prolonged and is followed by by:
disappearance of the P waves. a. Administering IV calcium gluconate-
 Finally, there is decomposition and prolongation of antagonizes action of K on cardiac conduction
the QRS complex. Ventricular dysrhythmias and b. Administering Insulin with dextrose-causes
cardiac arrest may occur at any point in this temporary shift of K into cells
progression. c. Administering sodium bicarbonate-alkalinizes
 Note that in Severe hyperkalemia causes muscle plasma to cause temporary shift
weakness and even paralysis, related to a d. Administering Beta-agonists
depolarization block in muscle. e. Administering Kayexalate (cation-exchange
 Similarly, ventricular conduction is slowed. resin)-draws K+ into the bowel
 Although hyperkalemia has marked effects on the NURSING MANAGEMENT
peripheral neuromuscular system, it has little effect on
the central nervous system. 1. Provide continuous monitoring of cardiac status,
 Rapidly ascending muscular weakness leading to dysrhythmias, and potassium levels.
flaccid quadriplegia has been reported in patients with 2. Assess for signs of muscular weakness, paresthesias,
very high serum potassium levels. nausea
 Paralysis of respiratory muscles and those required for 3. Evaluate and verify all HIGH serum K levels
phonation can also occur. 4. Prevent hyperkalemia by encouraging high risk patient
 Gastrointestinal manifestations, such as nausea, to adhere to proper potassium restriction
intermit tent intestinal colic, and diarrhea, may occur 5. Correct hyperkalemia by administering carefully
in hyperkalemic patients. prescribed drugs. Nurses must ensure that clients
receiving IVF with potassium must be always
monitored and that the potassium supplement is given
ASSESSMENT correctly
Physical Examination 6. Assist in hemodialysis if hyperkalemia cannot be
 Diarrhea corrected.
 Skeletal muscle weakness 7. Provide client teaching. Advise patients at risk to avoid
 Abnormal cardiac rate eating potassium rich foods, and to use potassium salts
Subjective Cues sparingly.
 Nausea 8. Monitor patients for hypokalemia who are receiving
 Intestinal pain/colic potassium-sparing diuretic
 Palpitations
Laboratory Findings CALCIUM
1. Peaked and narrow T waves
2. ST segment depression and shortened QT interval  Majority of calcium is in the bones and teeth
3. Prolonged PR interval  Small amount may be found in the ECF and ICF
4. Prolonged QRS complex  Normal serum range is 8.5 – 10.5 mg/dL
5. Disappearance of P wave  Sources: milk and milk products; diet; IVF and
6. Serum potassium is higher than 5.5 mEq/L medications
7. Acidosis


Functions: HYPOCALCEMIA
 Low levels of calcium in the blood
1. Needed for formation of bones and teeth
2. For muscular contraction and relaxation  Risk Factors
3. For neuronal and cardiac function a. Hypoparathyroidism (idiopathic or postsurgical)
4. For enzymatic activation b. Alkalosis (Ca binds to albumin)
5. For normal blood clotting c. Corticosteroids (antagonize Vit D)
d. Hyperphosphatemia
Regulations: e. Vit D deficiency
f. Renal failure (vit D deficiency)
1. GIT- absorbs Ca+ in the intestine; Vitamin D helps to
increase absorption  Clinical Manifestation
2. Renal regulation- Ca+ is filtered in the glomerulus  Decreased cardiac contractility
and reabsorbed in the tubules:  Arrhythmia
3. Endocrine regulation:  ECG: prolonged QT interval, lengthened ST
segment
 Parathyroid hormone from the parathyroid glands  Trousseau’s sign (inflate BP cuff 20mm above
is released when Ca+ level is low. PTH causes systole for 3 min = carpopedal spasm)
release of calcium from bones and increased
retention of calcium by the kidney but PO4 is
excreted
 Calcitonin from the thyroid gland is released when
the calcium level is high. This causes excretion of
both calcium and PO4 in the kidney and promoted
deposition of calcium in the bones.

 Chvostek’s sign (tap facial nerve anterior to the
ear = ipsilateral muscle twitching)

 Tetany
 Hyperreflexia, seizures
 Laryngeal spasms/stridor
 Diarrhea, hyperactive bowel sounds
 Bleeding

Collaborative Management
1. Calcium gluconate 10% IV
2. Calcium chloride 10% IV
3. both usually given by Dr, very slowly; venous irritant;
cardiac probs
4. Oral: calcium citrate, lactate, carbonate; Vit D
supplements
5. Diet: high calcium
6. Watch out for tetany, seizures, laryngospasm, resp &
cardiac arrest
7. Seizure precautions
Sources:
milk, yogurt, cheese, sardines, broccoli, tofu, green leafy
vegetables



HYPERCALCEMIA HYPOMAGNESEMIA

 is an elevated calcium level in the blood  is an electrolyte disturbance in which there is an
 usually from bone resorption abnormally low level of magnesium in the blood.

 Risk Factors / Causes  Risk Factors and Cause
a. Hyperparathyroidism (eg adenoma) a. Chronic alcoholism (most common), Alcohol
b. Metastatic cancer (bone resorption as tumor‟s stimulates renal excretion of magnesium,
ectopic PTH effect) – eg. Multiple myeloma b. Inflammatory bowel disease
c. Thiazide diuretics (potentiate PTH effect) c. Small bowel resection
d. Immobility d. GI cancer
e. Milk-alkali syndrome (too much milk or antacids e. chronic pancreatitis (poor absorption)
in aegs with peptic ulcer) f. Loop and thiazide diuretic use (the most common
cause of hypomagnesemia)
 Clinical Manifestation g. Antibiotics (i.e. aminoglycoside, amphotericin,
 groans (constipation) pentamidine, gentamicin, tobramycin, viomycin)
 moans (psychotic noise) block resorption in the loop of Henle.
 bones (bone pain, especially if PTH is elevated) h. Excess calcium
 stones (kidney stones) i. Excess saturated fats
 psychiatric overtones (including depression and j. Excess coffee or tea intake
confusion) k. Excess phosphoric or carbonic acids (soda pop)
l. Insufficient water consumption
 Arrhythmia m. Excess salt or sugar intake
 ECG: shortened QT interval, decreased ST n. Insufficient selenium,vitamin D, sunlight
segment exposure or vitamin B6
 Hyporeflexia, lethargy, coma o. Increased levels of stress

Collaborative Management  Clinical Manifestation
1. If parathyroid tumor = surgery  Weakness
2. Diet: low Ca, stop taking Ca Carbonate antacids,  muscle cramps
increase fluids  cardiac arrhythmia
3. IV flushing (usually NaCl)  increased irritability of the nervous system with
4. Loop diuretics tremors, athetosis, jerking, nystagmus and an
5. Corticosteroids extensor plantar reflex. Confusion
6. Biphosphonates, like etidronate (Calcitonin) &  disorientation
alendronate (Fosamax)  hallucinations
7. Plicamycin (Mithracin) – inhibits bone resorption  depression
8. Calcitonin – IM or intranasal  epileptic fits
9. Dialysis (severe case)  hypertension, tachycardia and tetany.
10. Watch out for digitalis toxicity
11. Prevent fractures, handle gently * Like hypocalcemia, hypokalemia
Potentiates digitalis toxicity

MAGNESIUM Collaborative Management
1. Magnesium sulfate IV, IM (make sure renal
function is ok) – may cause flushing
 2nd most abundant intracellular cation 2. Oral: Magnesium oxide 300mg/day,
 50% found in bone, 45% is intracellular 3. Mg-containing antacids (SE diarrhea)
 ATP (adenosine triphosphate), the main source of 4. Diet: high magnesium (fruits,green vegetables,
energy in cells, must be bound to a magnesium ion in whole grains cereals, milk, meat, nuts and sea
order to be biologically active. foods )
 competes with Ca & P absorption in the GI 5. Promotion of safety, protect from injury
 inhibits PTH
 Normal value : 1.5-2.5 mEq/L
HYPERMAGNESEMIA
Functions:
1. important in maintaining intracellular activity  Etiologic Factors
2. affects muscle contraction, & especially relaxation a. Magnesium treatment for pre-eclampsia
3. maintains normal heart rhythm b. Renal failure
4. promotes vasodilation of peripheral arterioles c. Diabetic Ketoacidosis
d. Excessive use of Mg antacids/laxatives
Sources:
green leafy vegetables, nuts, legumes, seafood, whole
grains, bananas, oranges, cocoa, chocolate PATHOPHYSIOLOGY
Increase Mg. ----- Blocks acetylcholine release ---- decrease
excitability of muscle



 Clinical Manifestation HYPERPHOSPHATEMIA
 Hyporeflexia
 Hypotension, bradycardia, arrhythmia  Risk Factors
 Flushing a. Acidosis (Ph moves out of cell)
 Weakness, lethargy, coma b. Cytotoxic agents/chemotherapy in cancer
 Decreased RR & respiratory paralysis c. Renal failure
 Loss of DTR‟s d. Hypocalcemia
e. Massive BT (P leaks out of cells during storage of
*like hypercalcemia blood)
f. Hyperthyroidism
1. Diuretics  Clinical Manifestation
2. Stop Mg-containing antacids & enemas  Calcification of kidney, cornea, heart
3. IV fluids rehydration  Muscle spasms, tetany, hyperreflexia
4. Calcium gluconate – (antidote, antagonizes
cardiac & respiratory effects of Mg) *like hypocalcemia
5. Dialysis – if RF

Collaborative ManagementM
PHOSPHORUS 1. Aluminum antacids as phosphate binders: Al
carbonate (Basaljel), Al hydroxide (Amphojel)
 primary intracellular anion 2. Ca carbonate for hypocalcemia
 part of ATP – energy 3. Avoid phosphate laxatives/enemas
 85% bound with Ca in teeth/bones, skeletal muscle 4. Increase fluid intake
 reciprocal balance with Ca 5. Diet: low Phos, no carbonated drinks
 absorption affected by Vit D, regulation affected by
PTH (lowers P level)
 Normal value : 2.5-4.5 mg/dL CHLORIDE

Functions:  extracellular anion, part of salt
1. bone/teeth formation & strength  binds with Na, H (also K, Ca, etc)
2. phospholipids (make up cell membrane integrity)  exchanges with HCO3 in the kidneys (& in RBCs)
3. part of ATP  Normal value: 95 -108 mEq/L
4. affects metabolism, Ca levels
Functions:
Sources: 1. helps regulate BP, serum osmolarity
red & organ meats (brain, liver, kidney), poultry, fish, eggs, 2. part of HCl
milk, legumes, whole grains, nuts, carbonated drinks 3. acid/base balance (exchanges with HCO3)

HYPOPHOSPHATEMIA Sources:
salt, canned food, cheese, milk, eggs, crab, olives
 Risk Factors
a. Decreased Vit D absorption, sunlight exposure
b. Hyperparathyroidism (increased PTH) HYPOCHLOREMIA
c. Aluminum & Mg-containing antacids (bind P)
d. Severe vomiting & diarrhea  Risk Factors
a. Diuresis
 Clinical Manifestation b. Metabolic alkalosis
 Anemia, bruising (weak blood cell membrane) c. Hyponatremia, prolonged D5W IV
 Seizures, coma d. Addison‟s
 Muscle weakness, paresthesias
 Constipation, hypoactive bowel sounds  Clinical Manifestation
 Slow, shallow respirations (met. Alkalosis)
*Like hypercalcemia  Hypotension (Na & water loss)

Collaborative Management Collaborative Management
1. Sodium phosphate or potassium phosphate IV 1. Administer IV or Oral : KCl, NaCl
(give slowly, no faster than 10 mEq/hr) 2. Diet: high Cl (& usually Na)
2. Sodium & potassium phosphate orally (Neutra-
Phos, K-Phos) – give with meals to prevent gastric
irritation HYPERCHLOREMIA
3. Avoid Phos-binding antacids
4. Diet: high Mg, milk  Risk Factors / Cause
5. Monitor joint stiffness, arthralgia, fractures, a. Metabolic acidosis
bleeding b. Usually noted in hyperNa, hyperK



 Clinical Manifestation Interpretation Arterial Blood Gases
 Deep, rapid respirations (met. Acidosis)
 hyperK, hyperNa S/S  If acidosis the pH is down
 Increased Cl sweat levels in cystic fibrosis  If alkalosis the pH is up
 The respiratory function indicator is the PCO2
 The metabolic function indicator is the HCO3
1. Diuretics Step 1
2. Hypotonic solutions, D5W to restore balance  Look at the pH
3. Diet: low Cl (& usually Na)  Is it up or down?
4. Treat acidosis  If it is up - it reflects alkalosis
 If it is down - it reflects acidosis

Step 2
 Look at the PCO2
 Is it up or down?
Acid-Base Balance Mechanisms  If it reflects an opposite response as the pH,
 then you know that the condition is a
respiratory imbalance
 If it does not reflect an opposite response as the
Buffer - prevents major changes in ECF by releasing or
pH - move to step III
accepting H ions
Step 3
Buffer mechanism: first line (takes seconds)
 Look at the HCO3
1. combine with very strong acids or bases to
 Does the HCO3 reflect a corresponding
convert them into weaker acids or bases
 response with the pH
2. Bicarbonate Buffer System
 If it does then the condition is a metabolic
- most important
imbalance
- uses HCO3 & carbonic acid/H2CO3 - (20:1)
- closely linked with respiratory & renal
mechanisms
3. Phosphate Buffer System FACTORS AFFECTING BODY FLUIDS,
- more important in intracellular fluids, where ELECTROLYTES AND ACID-BASE BALANCE
concentration is higher
- similar to bicarbonate buffer system, only uses AGE
phosphate  Infants have higher proportion of body water than
4. Protein Buffer System adults
- hemoglobin, a protein buffer, promotes  Water content of the body decreases with age
movement of chloride across RBC membrane in  Infants have higher fluid turn-over due to immature
exchange for HCO3 kidney and rapid respiratory rate

Respiratory mechanism: 2nd line (takes minutes)
1. increased respirations liberates more CO2 = GENDER AND BODY SIZE
increase pH  Women have higher body fat content but lesser
2. decreased respirations conserve more CO2 = water content
decrease pH  Lean body has higher water content
carbonic acid (H2CO3) = CO2 + water
ENVIRONMENT AND TEMPERATURE
Renal mechanism: 3rd line (takes hours-days)  Climate and heat and humidity affect fluid balance
1. kidneys secrete H ions & reabsorb bicarbonate ions =
increase blood pH
2. kidneys form ammonia that combines with H ions to DIET AND LIFESTYLE
form ammonium ions, which are excreted in the urine  Anorexia nervosa will lead to nutritional depletion
in exchange for sodium ions  Stressful situations will increase metabolism,
increase ADH causing water retention and
Review: Acid-Base Imbalance increased blood volume
 Chronic Alcohol consumption causes malnutrition
pH – 7.35-7.45
pCO2 – measurement of the CO2 pressure that is being ILLNESS
exerted on the plasma  Trauma and burns release K+ in the blood
- 35-45mmHg  Cardiac dysfunction will lead to edema and
PaO2- amount of pressure exerted by O2 on the plasma congestion
- 80-100mmHg
SaO2- percent of hemoglobin saturated with O2
Base excess – amount of HCO3 available in the ECF MEDICAL TREATMENT, MEDICATIONS AND
- -3 to +3 SURGERY
 Suctioning, diuretics and laxatives may cause
imbalances



Signs and Symptoms
ACID-BASE BALANCE PROBLEMS  Compensation: kidneys compensate by
eliminating bicarbonate ions; decrease in
bicarbonate HCO3 < 22 mm Hg.
 Respiratory: hyperventilating: shallow, rapid
RESPIRATORY ACIDOSIS breathing
 pH < 7.35  Neuro: panicked, light-headed, tremors, may
 pCO2 > 45 mm Hg (excess carbon dioxide in the develop tetany, numb hands and feet (related to
blood) symptoms of hypocalcemia; with elevated pH
 Respiratory system impaired and retaining CO2; more Ca ions are bound to serum albumin and less
causing acidosis ionized “active” calcium available for nerve and
muscle conduction)
Common Stimuli  May progress to seizures, loss of consciousness
a. Acute respiratory failure from airway obstruction (when normal breathing pattern returns)
b. Over-sedation from anesthesia or narcotics  Cardiac: palpitations, sensation of chest tightness
c. Some neuromuscular diseases that affect ability to
use chest muscles Collaborative Management
d. Chronic respiratory problems, such as Chronic
Obstructive Lung Disease 1. Treatment: encourage client to breathe slowly in a
paper bag to rebreathe CO2
Signs and Symptoms 2. Breathe with the patient; provide emotional
 Compensation: kidneys respond by generating and support and reassurance, anti-anxiety agents,
reabsorbing bicarbonate ions, so HCO3 >26 mm Hg sedation
 Respiratory: hypoventilation, slow or shallow 3. On ventilator, adjustment of ventilation settings
respirations (decrease rate and tidal volume)
 Neuro: headache, blurred vision, irritability, 4. Prevention: pre-procedure teaching, preventative
confusion emotional support, monitor blood gases as
 Respiratory collapse leads to unconsciousness and indicated
cardiovascular collapse

Collaborative Management METABOLIC ACIDOSIS
1. Early recognition of respiratory status and treat  pH <7.35
cause  Deficit of bicarbonate in the blood NaHCO3 <22
2. Restore ventilation and gas exchange; CPR for mEq/L
respiratory failure with oxygen supplementation;  Caused by an excess of acid, or loss of
intubation and ventilator support if indicated bicarbonate from the body
3. Treatment of respiratory infections with
bronchodilators, antibiotic therapy Common Stimuli
4. Reverse excess anesthetics and narcotics with a. Acute lactic acidosis from tissue hypoxia (lactic
medications such as naloxone (Narcan) acid produced from anaerobic metabolism with
5. Chronic respiratory conditions shock, cardiac arrest)
 Breathe in response to low oxygen levels b. Ketoacidosis (fatty acids are released and
 Adjusted to high carbon dioxide level converted to ketones when fat is used to supply
through metabolic compensation (therefore, glucose needs as in uncontrolled Type 1 diabetes
high CO2 not a breathing trigger) or starvation)
 Cannot receive high levels of oxygen, or will c. Acute or chronic renal failure (kidneys unable to
have no trigger to breathe; will develop regulate electrolytes)
carbon dioxide narcosis d. Excessive bicarbonate loss (severe diarrhea,
 Treat with no higher than 2 liters O2 per intestinal suction, bowel fistulas)
cannula e. Usually results from some other disease and is
6. Continue respiratory assessments, monitor further often accompanied by electrolyte and fluid
arterial blood gas results imbalances
f. Hyperkalemia often occurs as the hydrogen ions
enter cells to lower the pH displacing the
RESPIRATORY ALKALOSIS intracellular potassium; hypercalcemia and
 pH < 7.35 hypomagnesemia may occur
 pCO2 < 35 mm Hg.
 Carbon dioxide deficit, secondary to Signs and Symptoms
hyperventilation  Compensation: respiratory system begins to
compensate by increasing the depth and rate of
Common Stimuli respiration in an effort to lower the CO2 in the blood;
a. Hyperventilation with anxiety from uncontrolled this causes a decreased level of carbon dioxide: pCO2
fear, pain, stress (e.g. women in labor, trauma <35 mm HG.
victims)  Neuro changes: headache, weakness, fatigue
b. High fever progressing to confusion, stupor, and coma
c. Mechanical ventilation, during anesthesia  Cardiac: dysrhythmias and possibly cardiac arrest from
hyperkalemia
 GI: anorexia, nausea, vomiting
 Skin: warm and flushed



 Respiratory: tries to compensate by hyperventilation: 1. Correcting underlying cause will often improve
deep and rapid respirations known as Kussmaul‟s alkalosis
respirations 2. Restore fluid volume and correct electrolyte
imbalances (usually IV NaCl with KCL).
Diagnostic test findings: 3. With severe cases, acidifying solution may be
1. ABG: pH < 7.35, HCO3 < 22 administered.
2. Electrolytes: Serum K+ >5.0 mEq/L 4. Assessment
3. Serum Ca+2 > 10.0 mg/dL  Vital signs
4. Serum Mg+2 < 1.6 mg/dL  Neuro, cardiac, respiratory assessment
 Repeat arterial blood gases and electrolytes
1. Medications: Correcting underlying cause will
often improve acidosis
2. Restore fluid balance, prevent dehydration with
IV fluids
Selected Water and Electrolyte
3. Correct electrolyte imbalances Solutions
4. Administer Sodium Bicarbonate IV, if acidosis is
severe and does not respond rapidly enough to
treatment of primary cause. (Oral bicarbonate is
sometimes given to clients with chronic metabolic Isotonic Solutions
acidosis) Be careful not to overtreat and put client
into alkalosis A. 0.9% NaCl (isotonic, also called NSS)
5. As acidosis improves, hydrogen ions shift out of Na+ 154 mEq/L
cells and potassium moves intracellularly. Cl- 154 mEq/L
Hyperkalemia may become hypokalemia and (308 mOsm/L)
potassium replacement will be needed. Also available with varying concentrations of dextrose (the
6. Assessment most frequent used is a 5% dextrose concentration
 Vital signs
 Intake and output  An isotonic solution that expands the ECF
 Neuro, GI, and respiratory status; volume, used in hypovolemic states, resuscitative
 Cardiac monitoring efforts, shock, diabetic ketoacidosis, metabolic
 Reassess repeated arterial blood gases and alkalosis, hypercalcemia, mild Na deficit
electrolytes  Supplies an excess of Na and Cl; can cause fluid
volume excess and hyperchloremic acidosis if
used in excessive volumes, particularly in patients
METABOLIC ALKALOSIS with compromised renal function, heart failure or
 pH >7.45 edema
 HCO3 > 26 mEq/L  Not desirable as a routine maintenance solution,
 Caused by a bicarbonate excess, due to loss of as it provides only Na and Cl (and these are
acid, or a bicarbonate excess in the body provided in excessive amounts)
 When mixed with 5% dextrose, the resulting
Common Stimuli solution becomes hypertonic in relation to plasma,
a. Loss of hydrogen and chloride ions through and in addition to the above described
excessive vomiting, gastric suctioning, or electrolytes, provides 170cal/L
excessive diuretic therapy Response to  Only solution that may be administered with
hypokalemia blood products
b. Excess ingestion of bicarbonate rich antacids or
excessive treatment of acidosis with Sodium
Bicarbonate B. Lactated Ringer’s solution (Hartmann’s solution)
Na+ 130 mEq/L
Signs and Symptoms K+ 4 mEq/L
 Compensation: Lungs respond by decreasing the Ca++ 3 mEq/L
depth and rate of respiration in effort to retain carbon Cl- 109 mEq/L
dioxide and lower pH Lactate (metabolized to bicarbonate) 28 mEq/L (274
 Neuro: altered mental status, numbness and tingling mOsm/L)
around mouth, fingers, toes, dizziness, muscle spasms Also available with varying concentration of dextrose (the
(similar to hypocalcemia due to less ionized calcium most common is 5% dextrose)
levels)
 Respiratory: shallow, slow breathing  An isotonic solution that contains multiple
electrolytes in roughly the same concentration as
Diagnostic test findings found in plasma (note that solution is lacking in
1. ABG‟s: pH> 7.45, HCO3 >26 Mg++) provides 9 cal/L
2. Electrolytes: Serum K+ < 3.5 mEq/L  Used in the tx of hypovolemia, burns, fluid lost as
3. Electrocardiogram: as with hypokalemia bile or diarrhea, and for acute blood loss
replacement
 Lactate is rapidly metabolized into HCO3- in the
body. Lactated Ringer‟s solution should not be
used in lactic acidosis because the ability to
convert lactate into HCO3- is impaired in this
Collaborative Management disorder.


 Not to be given with a pH > 7.5 because Hypertonic Solutions
bicarbonates is formed as lactate breaks down
causing alkalosis E. 3% NaCl (hypertonic saline)
 Should not be used in renal failure because it Na+ 513 mEq/L
contains potassium and can cause hyperkalemia Cl- 513 mEq/L
 Similar to plasma (1026 mOsm/L)

 Used to increase ECF volume, decrease cellular
C. 5% Dextrose in Water (D5W) swelling
No electrolytes  Highly hypertonic solution used only in critical
50 g of glucose situations to treat hyponatremia
 Must be administered slowly and cautiously,
 An isotonic solution that supplies 170 cal/L and because it can cause intravascular volume
free water to aid in renal excretion of solutes overload and pulmonary edema
 Used in treatment of hypernatremia, fluid loss and  Supplies no calories
dehydration  Assists in removing ICF excess
 Should not be used in excessive volumes in the
early post-op period (when ADH secretion is F. 5% NaCl (hypertonic solution)
increased due to stress reaction) Na+ 855 mEq/L
 Should not be used solely in tx of fluid volume Cl- 855 mEq/L
deficit, because it dilutes plasma electrolyte (1710 mOsm/L)
concentrations
 Contraindicated in head injury because it may  Highly hypertonic solution used to treat
cause increased intracranial pressure symptomatic hyponatremia
 Should not be used for fluid resuscitation because  Administered slowly and cautiously, because it
it can cause hyperglycemia can cause intravascular volume overload and
 Should be used with caution in patients with renal pulmonary edema
or cardiac dse because of risk of fluid overload  Supplies no calories
 Electrolyte-free solutions may cause peripheral
circulatory collapse, anuria in pt. with sodium
deficiency and increased body fluid loss
 Converts to hypotonic solution as dextrose is Colloid Solutions
metabolized by body. Overtime D5W without
NaCl can cause water intoxication (ICF vol. G. Dextran in NS or 5% D5W
excess bec. solution is hypotonic) Available in low-molecular-weight (Dextran 40) and high-
molecular-weight (Dextran 70) forms

 Colloid solution used as volume/plasma expander
Hypotonic Solutions for intravascular part of ECF
 Affects clotting by coating platelets and
D. 0.45% NaCl decreasing ability to clot
half-strength saline)  Remains in circulatory system up to 24 hours
Na+ 77 mEq/L  Used to treat hypovolemia in early shock to
Cl- 77 mEq/L increase pulse pressure, CO, and arterial BP
(154 mOsm/L)  Improves microcirculation by decreasing RBC
Also available with varying concentration of dextrose (the aggregation
most common is 5% dextrose)  Contraindicated in hemorrhage,
thrombocytopenia, renal dse and severe
 Provides Na, Cl and free water dehydration
 Free water is desirable to aid the kidneys in  Not a substitute for blood or blood products
elimination of solute
 Lacking in electrolytes other than Na and Cl
 When mixed with 5% dextrose, the solution
becomes slightly hypertonic to plasma and in
addition to the above-described electrolytes
provides 170 cal/L
 Used in the tx of hypertonic dehydration, Na and
Cl depletion and gastric fluid loss
 Not indicated for third-space fluid shifts or
increased intracranial pressure
 Administer cautiously, because it can cause fluid
shifts from vascular system into cells, resulting in
cardiovascular collapse and increased intracranial
pressure


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