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

N,
MAN

STI COLLEGE GLOBAL CITY College of Nursing MEDICAL AND SURGICAL NURSING Fluids and
Electrolytes

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 normal range = 275-295 mOsm/kg of water osmolarity –
concentration of solute per L of solution * since 1kg=1L, & water is the solvent of
the human body, osmolarity & osmolality are used interchangeably

IV.

Lecturer: Mark Fredderick R. Abejo RN, MAN

________________________________________________ FLUIDS & ELECTROLYTES I. Fluid
Status of Human Body A. Homeostasis: state of the body when maintaining a state of
balance in the presence of constantly changing conditions B. Includes balance of
fluid, electrolytes, and acidbase balance C. Body water intake and output
approximately equal (2500 mL/24 hr.)

Adult body: 40L water, 60% body weight 2/3 intracellular 1/3 extracellular (80%
interstitial, 20% intravascular) Infant: 70-80% water Elderly: 40-50% water

Mechanisms of Body Fluid Movement (i.e. movement of solutes, solvents across

different extracellular locations) A. Osmosis: water is mover; water moves from
lower concentration to higher concentration 1. Normal Osmolality of ICF and ECF:
275 – 295 mOsm/kg 2. Types of solutions according to osmolality Isotonic: all
solutions with osmolality same as that of plasma .Body cells placed in isotonic
fluid: neither shrink nor swell Hypertonic: fluid with greater concentration of
solutes than plasma Cells in hypertonic solution: water in cells moves to outside
to equalize concentrations: cells will shrink Hypotonic: fluid with lower
concentration of solutes than plasma Cells in hypotonic solution: water outside
cells moves to inside of cells: cells will swell and eventually burst (hemolyze) 3.
Different intravenous solutions, used to correct some abnormal conditions,
categorized according to osmolality: B. Diffusion: solute molecules move from
higher concentration to lower concentration 1. Solute, such as electrolytes, is the
mover; not the water 2. Types: simple and facilitated (movement of large water-
soluble molecules) Filtration: water and solutes move from area of higher
hydrostatic pressure to lower hydrostatic pressure 1. Hydrostatic pressure is
created by pumping action of heart and gravity against capillary wall 2. Usually
occurs across capillary membranes Active Transport: molecules move across cell
membranes against concentration gradient; requires energy, e.g. Na – K pump

II. Body Fluid Composition A. Water: 60% of body weight B. Electrolytes: substances
that become charged particles in solution 1. Cations: positively charged (e.g. Na+,
K+) 2. Anions: negatively charged (e.g. Cl-) 3. Both are measured in
milliequivalents per liter (mEq/L) C. Balance of hydrostatic pressure and osmotic
pressure regulates movement of water between intravascular and interstitial spaces
III. Body Fluid Distribution: A. 2 body compartments: 1. Intracellular fluids
(ICF): fluids within cells of body [major intracellular electrolytes: Potassium
(K+), Magnesium (Mg +2)] 2. Extracellular fluids (ECF): fluid outside cells; [major
extracellular electrolytes: Sodium (Na+), Chloride(Cl-)]; this is where
transportation of nutrients, oxygen, and waste products occurs B. Locations of ECF:
1. Interstitial: fluid between most cells 2. Intravascular: fluid within blood
vessels; also called plasma 3. Transcellular: fluids of body including urine,
digestive secretion, cerebrospinal, pleural, synovial, intraocular, gonadal,
pericardial
C.

D.

Hydrostatic pressure -pushes fluid out of vessels into tissue space; higher to
lower pressure – due to water volume in vessels; greater in arterial end –
swelling: varicose veins, fluid overload, kidney failure & CHF Osmotic pressure
-pulls fluid into vessels; from weaker concentration to stronger concentration -
from plasma proteins; greater in venous end - swelling: liver problems, nephrotic
syndrome

MS: Fluids and Electrolyte

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

V.

Mechanisms that Regulate Homeostasis: How the body adapts to fluid and electrolyte
changes? A. B. Thirst: primary regulator of water intake (thirst center in brain)
Kidneys: regulator of volume and osmolality by controlling excretion of water and
electrolytes Renin-angiotension-aldosterone mechanism: response to a drop in blood
pressure; results from vasoconstriction and sodium regulation by aldosterone
Antidiuretic hormone: hormone to regulate water excretion; responds to osmolality
and blood volume Atrial natriuretic factor: hormone from atrial heart muscle in
response to fluid excess; causes increased urine output by blocking aldosterone

ADH – produced by hypothalamus, released by posterior pituitary when osmoreceptor

or baroreceptor is triggered in hypothalamus Aldosterone – produced by adrenal
cortex; promotes Na & water reabsorption

C.

Sensible & Insensible Fluid Loss Sensible: Insensible: urine, vomiting, suctioned
secretions lungs , skin, GI and evaporation

D.

E.

Normal Fluid Intake and Loss in Adults Intake:  Water in food  Water from
oxidation  Water in liquid TOTAL Output:     2,500 mls

Fluid Balance Regulation Thirst reflex triggered by: 1. decreased salivation & dry
mouth 2. increased osmotic pressure stimulates osmoreceptors in the hypothalamus 3.
decreased blood volume activates the renin/angiontensin pathway, which simulates
the thirst center in hypothalamus 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
MS: Fluids and Electrolyte

1,000 mls 300 mls 1,200 mls

Skin Lungs Feces Kidneys TOTAL

500 mls 300 mls 150 mls 1,500 mls 2,500 mls

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

IV Fluids Isotonic

 LR PNSS (0.9%NSS) NM D5W - isotonic in bag - dextrose=quickly

metabolized=hypotonic D2.5W 0.45% NSS 0.3% NSS 0.2% NSS D50W D10W D5NSS D5LR 3%NSS

Hypotonic

Risk factors are the following: a. Diabetes Insipidus b. Adrenal insufficiency c.

Osmotic diuresis d. Hemorrhage e. Coma f. Third-spacing conditions like ascites,
pancreatitis and burns

PATHOPHYSIOLOGY: Risk Factors --- inadequate fluids in the body ---- decreased
blood volume ----- decreased cellular hydration ---- cellular shrinkage ---- weight
loss, decreased turgor, oliguria, hypotension, weak pulse, etc.

Hypertonic

ASSESSMENT: Physical examination       Weight loss, tented skin turgor, dry

mucus membrane Hypotension Tachycardia Cool skin, acute weight loss Flat neck veins
Decreased CVP

Colloids (usually CHONs) & Plasma expanders Dextran – synthetic polysaccharide,

glucose solution increase concentration of blood, improving blood volume up to 24
hrs contraindicated: heart failure, pulmonary edema, cardiogenic shock, and renal
failure Hetastarch – like Dextran, but longer-acting expensive derived from corn
starch Composition of Fluids Saline solutions – water, Na, Cl Dextrose solutions –
water or saline, calories Lactated Ringer‟s – water, Na, Cl, K, Ca, lactate Plasma
expanders – albumin, dextran, plasma protein (plasmanate) - increases oncotic
pressure, pulling fluids into circulation Parenteral hyperalimentation – fluid,
electrolytes, amino acids, calories A. FLUID VOLUME DEFICIT or HYPOVOLEMIA 
Definition: This is the loss of extra cellular fluid volume that exceeds the intake
of fluid. The loss of water and electrolyte is in equal proportion. It can be
called in various terms- vascular, cellular or intracellular dehydration. But the
preferred term is hypovolemia. Dehydration refers to loss of WATER alone, with
increased solutes concentration and sodium concentration

Subjective cues     Thirst Nausea, anorexia Muscle weakness and cramps Change
in mental state

Laboratory findings 1. 2. 3. 4. Elevated BUN due to depletion of fluids or

decreased renal perfusion Hemoconcentration Possible Electrolyte imbalances:
Hypokalemia, Hyperkalemia, Hyponatremia, hypernatremia Urine specific gravity is
increased (concentrated urine) above 1.020

NURSING MANAGEMENT 1. 2. 3. Assess the ongoing status of the patient by doing an

accurate input and output monitoring Monitor daily weights. Approximate weight loss
1 kilogram = 1liter! Monitor Vital signs, skin and tongue turgor, urinary
concentration, mental function and peripheral circulation Prevent Fluid Volume
Deficit from occurring by identifying risk patients and implement fluid replacement
therapy as needed promptly Correct fluid Volume Deficit by offering fluids orally
if tolerated, anti-emetics if with vomiting, and foods with adequate electrolytes
Maintain skin integrity Provide frequent oral care Teach patient to change position
slowly to avoid sudden postural hypotension


Pathophysiology of Fluid Volume Deficit  Etiologic conditions include: a. Vomiting
b. Diarrhea c. Prolonged GI suctioning d. Increased sweating e. Inability to gain
access to fluids f. Inadequate fluid intake g. Massive third spacing

4.

5.

6. 7. 8.

MS: Fluids and Electrolyte

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

B.

FLUID VOLUME EXCESS: HYPERVOLEMIA  Definition : Refers to the isotonic expansion

of the ECF caused by the abnormal retention of water and sodium  There is
excessive retention of water and electrolytes in equal proportion. Serum sodium
concentration remains NORMAL

4.

5.

Teach patient about edema, ascites, and fluid therapy. Advise elevation of the
extremities, restriction of fluids, necessity of paracentesis, dialysis and
diuretic therapy. Instruct patient to avoid over-the-counter medications without
first checking with the health care provider because they may contain sodium

Pathophysiology of Fluid Volume Excess  Etiologic conditions and Risks factors a.

Congestive heart failure b. Renal failure c. Excessive fluid intake d. Impaired
ability to excrete fluid as in renal disease e. Cirrhosis of the liver f.
Consumption of excessive table salts g. Administration of excessive IVF h. Abnormal
fluid retention ELECTROLYTES  Electrolytes are charged ions capable of conducting
electricity and are solutes found in all body compartments.

Sources of electrolytes  Foods and ingested fluids, medications; IVF and TPN
solutions

PATHOPHYSIOLOGY Excessive fluid --- expansion of blood volume ----- edema,

increased neck vein distention, tachycardia, hypertension.

Functions of Electrolytes  Maintains fluid balance  Regulates acid-base balance 

Needed for enzymatic secretion and activation  Needed for proper metabolism and
effective processes of muscular contraction, nerve transmission Types of
Electrolytes  CATIONS- positively charged ions; examples are sodium, potassium,
calcium  ANIONS- negatively charged ions; examples are chloride and phosphates] 
The major ICF cation is potassium (K+); the major ICF anion is Phosphates  The
major ECF cation is Sodium (Na+); the major ECF anion is Chloride (Cl-)

The Nursing Process in Fluid Volume Excess ASSESSMENT Physical Examination 

Increased weight gain  Increased urine output  Moist crackles in the lungs 
Increased CVP  Distended neck veins  Wheezing  Dependent edema Subjective cue/s
 Shortness of breath  Change in mental state Laboratory findings 1. BUN and
Creatinine levels are LOW because of dilution 2. Urine sodium and osmolality
decreased (urine becomes diluted) 3. CXR may show pulmonary congestion
IMPLEMENTATION ASSIST IN MEDICAL INTERVENTION 1. 2. 3. Administer diuretics as
prescribed Assist in hemodialysis Provide dietary restriction of sodium and water

ELECTROLYTE IMBALANCES

SODIUM    The most abundant cation in the ECF Normal range in the blood is 135-
145 mEq/L A loss or gain of sodium is usually accompanied by a loss or gain of
water.  Major contributor of the plasma Osmolality  Sources: Diet, medications,
IVF. The minimum daily requirement is 2 grams Functions: 1. 2. 3. 4. 5. 6. 7.
Participates in the Na-K pump Assists in maintaining blood volume Assists in nerve
transmission and muscle contraction Primary determinant of ECF concentration.
Controls water distribution throughout the body. Primary regulator of ECF volume.
Sodium also functions in the establishment of the electrochemical state necessary
for muscle contraction and the transmission of nerve impulses. Regulations: skin,
GIT, GUT, Aldosterone increases Na retention in the kidney

NURSING MANAGEMENT 1. Continually assess the patient‟s condition by measuring

intake and output, daily weight monitoring, edema assessment and breath sounds
Prevent Fluid Volume Excess by adhering to diet prescription of low salt- foods.
Detect and Control Fluid Volume Excess by closely monitoring IVF therapy,
administering medications, providing rest periods, placing in semi-fowler‟s
position for lung expansion and providing frequent skin care for the edema

2. 3.

8.

MS: Fluids and Electrolyte

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

SODIUM DEFICIT: HYPONATREMIA  Definition : Refers to a Sodium serum level of less

than 135 mEq/L. This may result from excessive sodium loss or excessive water gain.

In summary: Physical Examination  Altered mental status  Vomiting  Lethargy 

Muscle twitching and convulsions (if sodium level is below 115 mEq/L)  Focal
weakness Subjective Cues  Nausea  Cramps  Anorexia  Headache Laboratory
findings 1. Serum sodium level is less than 135 mEq/L 2. Decreased serum osmolality
3. Urine specific gravity is LOW if caused by sodium loss 4. In SIADH, urine sodium
is high and specific gravity is HIGH IMPLEMENTATION ASSIST IN MEDICAL INTERVENTION
1. Provide sodium replacement as ordered. Isotonic saline is usually ordered..
Infuse the solution very cautiously. The serum sodium must NOT be increased by
greater than 12 mEq/L because of the danger of pontine osmotic demyelination 2.
Administer lithium and demeclocycline in SIADH 3. Provide water restriction if with
excess volume NURSING MANAGEMENT 1. Provide continuous assessment by doing an
accurate intake and output, daily weights, mental status examination, urinary
sodium levels and GI manifestations. Maintain seizure precaution Detect and control
Hyponatremia by encouraging food intake with high sodium content, monitoring
patients on lithium therapy, monitoring input of fluids like IVF, parenteral
medication and feedings. Return the Sodium level to Normal by restricting water
intake if the primary problem is water retention. Administer sodium to normovolemic
patient and elevate the sodium slowly by using sodium chloride solution

Pathophysiology Etiologic Factors a. Fluid loss such as from Vomiting and

nasogastric suctioning b. Diarrhea c. Sweating d. Use of diuretics e. Fistula Other
factors a. Dilutional hyponatremia Water intoxication, compulsive water drinking
where sodium level is diluted with increased water intake b. SIADH Excessive
secretion of ADH causing water retention and dilutional hyponatremia
PATHOPHYSIOLOGY Decrease sodium concentration --- hypotonicity of plasma -- water
from the intravascular space will move out and go to the intracellular compartment
with a higher concentration --cell swelling --Water is pulled INTO the cell because
of decreased extracellular sodium level and increased intracellular concentration
The Nursing Process in HYPONATREMIA ASSESSMENT Sodium Deficit (Hyponatremia)
Clinical Manifestations  Clinical manifestations of hyponatremia depend on the
cause, magnitude, and rapidity of onset.  Although nausea and abdominal cramping
occur, most of the symptoms are neuropsychiatric and are probably related to the
cellular swelling and cerebral edema associated with hyponatremia.  As the
extracellular sodium level decreases, the cellular fluid becomes relatively more
concentrated and „pulls” water into the cells.  In general, those patients having
acute decline in serum sodium levels have more severe symptoms and higher mortality
rates than do those with more slowly developing hyponatremia.  Features of
hyponatremia associated with sodium loss and water gain include anorexia, muscle
cramps, and a feeling of exhaustion.  When the serum sodium level drops below 115
mEq/L (SI: 115 mmol/L), thee ff signs of increasing intracranial pressure occurs: 
lethargy  Confusion  muscular twitching  focal weakness  hemiparesis 
papilledema  convulsions

2.

3.

SODIUM EXCESS: HYPERNATREMIA   Serum Sodium level is higher than 145 mEq/L There
is a gain of sodium in excess of water or a loss of water in excess of sodium.

Pathophysiology: Etiologic factors a. Fluid deprivation b. Water loss from Watery

diarrhea, fever, and hyperventilation c. Administration of hypertonic solution d.
Increased insensible water loss e. Inadequate water replacement, inability to
swallow f. Seawater ingestion or excessive oral ingestion of salts

MS: Fluids and Electrolyte

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

Other factors a. Diabetes insipidus b. Heat stroke c. Near drowning in ocean d.

Malfunction of dialysis

IMPLEMENTATION ASSIST IN THE MEDICAL INTERVENTION 1. 2. Administer hypotonic

electrolyte solution slowly as ordered Administer diuretics as ordered Loop
diuretics (thiazides ok) Desmopressin is prescribed for diabetes insipidus

PATHOPHYSIOLOGY Increased sodium concentration --- hypertonic plasma ---water will

move out form the cell outside to the interstitial space ----- CELLULAR SHRINKAGE
----- then to the blood ---- Water pulled from cells because of increased
extracellular sodium level and decreased cellular fluid concentration

3.

NURSING MANAGEMENT 1. Continuously monitor the patient by assessing abnormal loses

of water, noting for the thirst and elevated body temperature and behavioral
changes Prevent hypernatremia by offering fluids regularly and plan with the
physician alternative routes if oral route is not possible. Ensure adequate water
for patients with DI. Administer IVF therapy cautiously Correct the Hypernatremia
by monitoring the patient‟s response to the IVF replacement. Administer the
hypotonic solution very slowly to prevent sudden cerebral edema. Monitor serum
sodium level. Reposition client regularly, keep side-rails up, the bed in low
position and the call bell/light within reach. Provide teaching to avoid over-the
counter medications without consultation as they may contain sodium

2.

The Nursing Process in HYPERNATREMIA Sodium Excess (Hypernatremia) Clinical

Manifestations  primarily neurologic  Presumably the consequence of cellular
dehydration.  Hypernatremia results in a relatively concentrated ECF, causing
water to be pulled from the cells.  Clinically, these changes may be manifested
by: o restlessness and weakness in moderate hypernatremia o disorientation,
delusions, and 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 can occur
(especially in children). Brain damage is apparently due to subarachnoid
hemorrhages that result from brain contraction. A primary characteristic of
hypernatremia is thirst. Thirst is so strong a defender of serum sodium levels in
normal people that hypernatremia never occurs unless the person is unconscious or
is denied access to water; unfortunately, ill people may have an impaired thirst
mechanism. Other signs include dry, swollen tongue and sticky mucous membranes. A
mild elevation in body temperature may occur, but on correction of the
hypernatremia the body temperature should return to normal. ASSESSMENT Physical
Examination  Restlessness, elevated body temperature  Disorientation  Dry,
swollen tongue and sticky mucous membrane, tented skin turgor  Flushed skin,
postural hypotension  Increased muscle tone and deep reflexes  Peripheral and
pulmonary edema Subjective Cues  Delusions and hallucinations  Extreme thirst 
Behavioral changes Laboratory findings 1. Serum sodium level exceeds 145 mEq/L 2.
Serum osmolality exceeds 295 mOsm/kg 3. Urine specific gravity and osmolality
INCREASED or elevated
MS: Fluids and Electrolyte

3.

4. 5. 6.
POTASSIUM      

 

The most abundant cation in the ICF Potassium is the major intracellular
electrolyte; in fact, 98% of the body‟s potassium is inside the cells. The
remaining 2% is in the ECF; it is this 2% that is all-important in neuromuscular
function. Potassium is constantly moving in and out of cells according to the
body‟s needs, under the influence of the sodium-potassium pump. Normal range in the
blood is 3.5-5 mEq/L Normal renal function is necessary for maintenance of
potassium balance, because 80-90% of the potassium is excreted daily from the body
by way of the kidneys. The other less than 20% is lost through the bowel and sweat
glands. Major electrolyte maintaining ICF balance Sources- Diet, vegetables,
fruits, IVF, medications

Functions: 1. 2. 3. 4. 5. Maintains ICF Osmolality Important for nerve conduction

and muscle contraction Maintains acid-base balance Needed for metabolism of
carbohydrates, fats and proteins Potassium influences both skeletal and cardiac
muscle activity. ( For example, alterations in its concentration change myocardial
irritability and rhythm ) Regulations: renal secretion and excretion, * Aldosterone
promotes renal excretion * Acidosis promotes K exchange for hydrogen

6.

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

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 Decreased
potassium in the body impaired nerve excitation and transmission signs/symptoms
such as weakness, cardiac dysrhythmias etc.. The Nursing Process in Hypokalemia 3.

IMPLEMENTATION ASSIST IN THE MEDICAL INTERVENTION 1. 2. Provide oral or IV

replacement of potassium Infuse parenteral potassium supplement. Always dilute the
K in the IVF solution and administer with a pump. IVF with potassium should be
given no faster than 1020-mEq/ hour! NEVER administer K by IV bolus or IM

Clinical Manifestations  Potassium deficiency can result in widespread

derangements in physiologic functions and especially nerve conduction.  Most
important, severe hypokalemia can result in death through cardiac or respiratory
arrest.  Clinical signs rarely develop before the serum potassium level has fallen
below 3 mEq/L (51: 3 mmol/L) unless the rate of fall has been rapid. 
Manifestations of hypokalemia include fatigue, anorexia, nausea, vomiting, muscle
weakness, decreased bowel motility, paresthesias, dysrhythmias, and increased
sensitivity to digitalis.  If prolonged, hypokalemia can lead to impaired renal
concentrating ability, causing dilute urine, polyuria, nocturia, and polydipsia
ASSESSMENT Physical examination  Muscle weakness  Decreased bowel motility and
abdominal distention  Paresthesias  Dysrhythmias  Increased sensitivity to
digitalis Subjective cues  Nausea , anorexia and vomiting  Fatigue, muscles
cramps  Excessive thirst, if severe Laboratory findings 1. Serum potassium is less
than 3.5 mEq/L 2. ECG: FLAT “T” waves, or inverted T waves, depressed ST segment
and presence of the “U” wave and prolonged PR interval. 3. Metabolic alkalosis
MS: Fluids and Electrolyte

NURSING MANAGEMENT 1. Continuously monitor the patient by assessing the cardiac

status, ECG monitoring, and digitalis precaution Prevent hypokalemia by encouraging
the patient to eat potassium rich foods like orange juice, bananas, cantaloupe,
peaches, potatoes, dates and apricots. Correct hypokalemia by administering
prescribed IV potassium replacement. The nurse must ensure that the kidney is
functioning properly! Administer IV potassium no faster than 20 mEq/hour and hook
the patient on a cardiac monitor. To EMPHASIZE: Potassium should NEVER be given IV
bolus or IM!! A concentration greater than 60 mEq/L is not advisable for peripheral
veins.

2.

3.

4.

5.

POTASSIUM EXCESS: HYPERKALEMIA  Serum potassium greater than 5.5 mEq/L

Pathophysiology  Etiologic factors a. Iatrogenic, excessive intake of potassium
b. Renal failure- decreased renal excretion of potassium c. Hypoaldosteronism and
Addison‟s disease d. Improper use of potassium supplements Other factors 1.
Pseudohyperkalemia- tight tourniquet and hemolysis of blood sample, marked
leukocytosis
Abejo

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

2. 3. 4.

Transfusion of “old” banked blood Acidosis 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.  The earliest changes, often occurring
at a serum potassium level greater than 6 mEq/ L (SI: 6 mmol/L), are peaked narrow
T waves and a shortened QT interval.  If the serum potassium level continues to
rise, the PR interval becomes prolonged and is followed by disappearance of the P
waves.  Finally, there is decomposition and prolongation of the QRS complex.
Ventricular dysrhythmias and cardiac arrest may occur at any point in this
progression.  Note that in Severe hyperkalemia causes muscle weakness and even
paralysis, related to a depolarization block in muscle.  Similarly, ventricular
conduction is slowed.  Although hyperkalemia has marked effects on the peripheral
neuromuscular system, it has little effect on the central nervous system.  Rapidly
ascending muscular weakness leading to flaccid quadriplegia has been reported in
patients with very high serum potassium levels.  Paralysis of respiratory muscles
and those required for phonation can also occur.  Gastrointestinal manifestations,
such as nausea, intermit tent intestinal colic, and diarrhea, may occur in
hyperkalemic patients. ASSESSMENT Physical Examination  Diarrhea  Skeletal muscle
weakness  Abnormal cardiac rate Subjective Cues  Nausea  Intestinal pain/colic 
Palpitations Laboratory Findings 1. Peaked and narrow T waves 2. ST segment
depression and shortened QT interval 3. Prolonged PR interval 4. Prolonged QRS
complex 5. Disappearance of P wave 6. Serum potassium is higher than 5.5 mEq/L 7.
Acidosis
MS: Fluids and Electrolyte

IMPLEMENTATION ASSIST IN MEDICAL INTERVENTION 1. Monitor the patient‟s cardiac

status with cardiac machine 2. Institute emergency therapy to lower potassium level
by: a. Administering IV calcium gluconateantagonizes action of K on cardiac
conduction b. Administering Insulin with dextrose-causes temporary shift of K into
cells c. Administering sodium bicarbonate-alkalinizes plasma to cause temporary
shift d. Administering Beta-agonists e. Administering Kayexalate (cation-exchange
resin)-draws K+ into the bowel NURSING MANAGEMENT 1. 2. 3. 4. 5. Provide continuous
monitoring of cardiac status, dysrhythmias, and potassium levels. Assess for signs
of muscular weakness, paresthesias, nausea Evaluate and verify all HIGH serum K
levels Prevent hyperkalemia by encouraging high risk patient to adhere to proper
potassium restriction Correct hyperkalemia by administering carefully prescribed
drugs. Nurses must ensure that clients receiving IVF with potassium must be always
monitored and that the potassium supplement is given correctly Assist in
hemodialysis if hyperkalemia cannot be corrected. Provide client teaching. Advise
patients at risk to avoid eating potassium rich foods, and to use potassium salts
sparingly. Monitor patients for hypokalemia who are receiving potassium-sparing
diuretic CALCIUM     Majority of calcium is in the bones and teeth Small amount
may be found in the ECF and ICF Normal serum range is 8.5 – 10.5 mg/dL Sources:
milk and milk products; diet; IVF and medications
Abejo
6. 7.

8.
Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N,
MAN

Functions: 1. 2. 3. 4. 5. Needed for formation of bones and teeth For muscular

contraction and relaxation For neuronal and cardiac function For enzymatic
activation For normal blood clotting

HYPOCALCEMIA  Low levels of calcium in the blood  Risk Factors a.

Hypoparathyroidism (idiopathic or postsurgical) b. Alkalosis (Ca binds to albumin)
c. Corticosteroids (antagonize Vit D) d. Hyperphosphatemia e. Vit D deficiency f.
Renal failure (vit D deficiency) Clinical Manifestation  Decreased cardiac
contractility  Arrhythmia  ECG: prolonged QT interval, lengthened ST segment 
Trousseau’s sign (inflate BP cuff 20mm above systole for 3 min = carpopedal spasm)

Regulations: 1. 2. 3. GIT- absorbs Ca+ in the intestine; Vitamin D helps to

increase absorption Renal regulation- Ca+ is filtered in the glomerulus and
reabsorbed in the tubules: Endocrine regulation:  Parathyroid hormone from the
parathyroid glands is released when Ca+ level is low. PTH causes 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

MS: Fluids and Electrolyte

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

HYPERCALCEMIA    is an elevated calcium level in the blood usually from bone

resorption Risk Factors / Causes a. Hyperparathyroidism (eg adenoma) b. Metastatic
cancer (bone resorption as tumor‟s ectopic PTH effect) – eg. Multiple myeloma c.
Thiazide diuretics (potentiate PTH effect) d. Immobility e. Milk-alkali syndrome
(too much milk or antacids in aegs with peptic ulcer) Clinical Manifestation 
groans (constipation)  moans (psychotic noise)  bones (bone pain, especially if
PTH is elevated)  stones (kidney stones)  psychiatric overtones (including
depression and confusion)    Arrhythmia ECG: shortened QT interval, decreased ST
segment Hyporeflexia, lethargy, coma

HYPOMAGNESEMIA   is an electrolyte disturbance in which there is an abnormally

low level of magnesium in the blood. Risk Factors and Cause a. Chronic alcoholism
(most common), Alcohol stimulates renal excretion of magnesium, b. Inflammatory
bowel disease c. Small bowel resection d. GI cancer e. chronic pancreatitis (poor
absorption) f. Loop and thiazide diuretic use (the most common cause of
hypomagnesemia) g. Antibiotics (i.e. aminoglycoside, amphotericin, pentamidine,
gentamicin, tobramycin, viomycin) block resorption in the loop of Henle. h. Excess
calcium i. Excess saturated fats j. Excess coffee or tea intake k. Excess
phosphoric or carbonic acids (soda pop) l. Insufficient water consumption m. Excess
salt or sugar intake n. Insufficient selenium,vitamin D, sunlight exposure or
vitamin B6 o. Increased levels of stress Clinical Manifestation  Weakness  muscle
cramps  cardiac arrhythmia  increased irritability of the nervous system with
tremors, athetosis, jerking, nystagmus and an extensor plantar reflex. Confusion 
disorientation  hallucinations  depression  epileptic fits  hypertension,
tachycardia and tetany. * Like hypocalcemia, hypokalemia Potentiates digitalis
toxicity Collaborative Management 1. Magnesium sulfate IV, IM (make sure renal
function is ok) – may cause flushing 2. Oral: Magnesium oxide 300mg/day, 3. Mg-
containing antacids (SE diarrhea) 4. Diet: high magnesium (fruits,green vegetables,
whole grains cereals, milk, meat, nuts and sea foods ) 5. Promotion of safety,
protect from injury

Collaborative Management 1. If parathyroid tumor = surgery 2. Diet: low Ca, stop

taking Ca Carbonate antacids, increase fluids 3. IV flushing (usually NaCl) 4. Loop
diuretics 5. Corticosteroids 6. Biphosphonates, like etidronate (Calcitonin) &
alendronate (Fosamax) 7. Plicamycin (Mithracin) – inhibits bone resorption 8.
Calcitonin – IM or intranasal 9. Dialysis (severe case) 10. Watch out for digitalis
toxicity 11. Prevent fractures, handle gently

MAGNESIUM       2nd most abundant intracellular cation 50% found in bone, 45%
is intracellular ATP (adenosine triphosphate), the main source of energy in cells,
must be bound to a magnesium ion in order to be biologically active. competes with
Ca & P absorption in the GI inhibits PTH Normal value : 1.5-2.5 mEq/L

HYPERMAGNESEMIA  Etiologic Factors a. Magnesium treatment for pre-eclampsia b.

Renal failure c. Diabetic Ketoacidosis d. Excessive use of Mg antacids/laxatives

Functions: 1. important in maintaining intracellular activity 2. affects muscle

contraction, & especially relaxation 3. maintains normal heart rhythm 4. promotes
vasodilation of peripheral arterioles Sources: green leafy vegetables, nuts,
legumes, seafood, whole grains, bananas, oranges, cocoa, chocolate

PATHOPHYSIOLOGY Increase Mg. ----- Blocks acetylcholine release ---- decrease

excitability of muscle

MS: Fluids and Electrolyte

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

Clinical Manifestation  Hyporeflexia  Hypotension, bradycardia, arrhythmia 

Flushing  Weakness, lethargy, coma  Decreased RR & respiratory paralysis  Loss
of DTR‟ s *like hypercalcemia

HYPERPHOSPHATEMIA  Risk Factors a. Acidosis (Ph moves out of cell) b. Cytotoxic

agents/chemotherapy in cancer c. Renal failure d. Hypocalcemia e. Massive BT (P
leaks out of cells during storage of blood) f. Hyperthyroidism Clinical
Manifestation  Calcification of kidney, cornea, heart  Muscle spasms, tetany,
hyperreflexia *like hypocalcemia

Collaborative Management 1. Diuretics 2. Stop Mg-containing antacids & enemas 3. IV

fluids rehydration 4. Calcium gluconate – (antidote, antagonizes cardiac &
respiratory effects of Mg) 5. Dialysis – if RF

PHOSPHORUS       primary intracellular anion part of ATP – energy 85% bound

with Ca in teeth/bones, skeletal muscle reciprocal balance with Ca absorption
affected by Vit D, regulation affected by PTH (lowers P level) Normal value : 2.5-
4.5 mg/dL

Collaborative ManagementM 1. Aluminum antacids as phosphate binders: Al carbonate

(Basaljel), Al hydroxide (Amphojel) 2. Ca carbonate for hypocalcemia 3. Avoid
phosphate laxatives/enemas 4. Increase fluid intake 5. Diet: low Phos, no
carbonated drinks

CHLORIDE     extracellular anion, part of salt binds with Na, H (also K, Ca,
etc) exchanges with HCO3 in the kidneys (& in RBCs) Normal value: 95 -108 mEq/L

Functions: 1. bone/teeth formation & strength 2. phospholipids (make up cell

membrane integrity) 3. part of ATP 4. affects metabolism, Ca levels Sources: red &
organ meats (brain, liver, kidney), poultry, fish, eggs, milk, legumes, whole
grains, nuts, carbonated drinks

Functions: 1. helps regulate BP, serum osmolarity 2. part of HCl 3. acid/base

balance (exchanges with HCO3)

HYPOPHOSPHATEMIA  Risk Factors a. Decreased Vit D absorption, sunlight exposure b.

Hyperparathyroidism (increased PTH) c. Aluminum & Mg-containing antacids (bind P)
d. Severe vomiting & diarrhea Clinical Manifestation  Anemia, bruising (weak blood
cell membrane)  Seizures, coma  Muscle weakness, paresthesias  Constipation,
hypoactive bowel sounds *Like hypercalcemia Collaborative Management 1. Sodium
phosphate or potassium phosphate IV (give slowly, no faster than 10 mEq/hr) 2.
Sodium & potassium phosphate orally (NeutraPhos, K-Phos) – give with meals to
prevent gastric irritation 3. Avoid Phos-binding antacids 4. Diet: high Mg, milk 5.
Monitor joint stiffness, arthralgia, fractures, bleeding

Sources: salt, canned food, cheese, milk, eggs, crab, olives

HYPOCHLOREMIA  Risk Factors a. Diuresis b. Metabolic alkalosis c. Hyponatremia,

prolonged D5W IV d. Addison‟ s Clinical Manifestation  Slow, shallow respirations
(met. Alkalosis)  Hypotension (Na & water loss)




Collaborative Management 1. Administer IV or Oral : KCl, NaCl 2. Diet: high Cl (&

usually Na)

HYPERCHLOREMIA  Risk Factors / Cause a. Metabolic acidosis b. Usually noted in

hyperNa, hyperK

MS: Fluids and Electrolyte

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

Clinical Manifestation  Deep, rapid respirations (met. Acidosis)  hyperK, hyperNa

S/S  Increased Cl sweat levels in cystic fibrosis

Interpretation Arterial Blood Gases     Step 1     Step 2     If

acidosis the pH is down If alkalosis the pH is up The respiratory function
indicator is the PCO2 The metabolic function indicator is the HCO3

Collaborative Management 1. Diuretics 2. Hypotonic solutions, D5W to restore

balance 3. Diet: low Cl (& usually Na) 4. Treat acidosis

Look at the pH Is it up or down? If it is up - it reflects alkalosis If it is down

- it reflects acidosis

Acid-Base Balance Mechanisms

Buffer - prevents major changes in ECF by releasing or accepting H ions Buffer
mechanism: first line (takes seconds) 1. combine with very strong acids or bases to
convert them into weaker acids or bases 2. Bicarbonate Buffer System - most
important - uses HCO3 & carbonic acid/H2CO3 - (20:1) - closely linked with
respiratory & renal mechanisms 3. Phosphate Buffer System - more important in
intracellular fluids, where concentration is higher - similar to bicarbonate buffer
system, only uses phosphate 4. Protein Buffer System - hemoglobin, a protein
buffer, promotes movement of chloride across RBC membrane in exchange for HCO3
Respiratory mechanism: 2nd line (takes minutes) 1. increased respirations liberates
more CO2 = increase pH 2. decreased respirations conserve more CO2 = decrease pH
carbonic acid (H2CO3) = CO2 + water Renal mechanism: 3rd line (takes hours-days) 1.
kidneys secrete H ions & reabsorb bicarbonate ions = increase blood pH 2. kidneys
form ammonia that combines with H ions to form ammonium ions, which are excreted in
the urine in exchange for sodium ions Review: Acid-Base Imbalance pH – 7.35-7.45
pCO2 – measurement of the CO2 pressure that is being exerted on the plasma 35-
45mmHg PaO2- amount of pressure exerted by O2 on the plasma 80-100mmHg SaO2-
percent of hemoglobin saturated with O2 Base excess – amount of HCO3 available in
the ECF -3 to +3

Look at the PCO2 Is it up or down? 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 pH - move to step III

Step 3    

Look at the HCO3 Does the HCO3 reflect a corresponding response with the pH If it
does then the condition is a metabolic imbalance

FACTORS AFFECTING BODY FLUIDS, ELECTROLYTES AND ACID-BASE BALANCE AGE   

Infants have higher proportion of body water than adults Water content of the body
decreases with age Infants have higher fluid turn-over due to immature kidney and
rapid respiratory rate

GENDER AND BODY SIZE  Women have higher body fat content but lesser water content
 Lean body has higher water content ENVIRONMENT AND TEMPERATURE  Climate and heat
and humidity affect fluid balance DIET AND LIFESTYLE  Anorexia nervosa will lead
to nutritional depletion  Stressful situations will increase metabolism, increase
ADH causing water retention and increased blood volume  Chronic Alcohol
consumption causes malnutrition ILLNESS  Trauma and burns release K+ in the blood
 Cardiac dysfunction will lead to edema and congestion MEDICAL TREATMENT,
MEDICATIONS AND SURGERY  Suctioning, diuretics and laxatives may cause imbalances
Abejo

MS: Fluids and Electrolyte

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

ACID-BASE BALANCE PROBLEMS

RESPIRATORY ACIDOSIS  pH < 7.35  pCO2 > 45 mm Hg (excess carbon dioxide in the
blood)  Respiratory system impaired and retaining CO2; causing acidosis Common
Stimuli a. Acute respiratory failure from airway obstruction b. Over-sedation from
anesthesia or narcotics c. Some neuromuscular diseases that affect ability to use
chest muscles d. Chronic respiratory problems, such as Chronic Obstructive Lung
Disease Signs and Symptoms  Compensation: kidneys respond by generating and
reabsorbing bicarbonate ions, so HCO3 >26 mm Hg  Respiratory: hypoventilation,
slow or shallow respirations  Neuro: headache, blurred vision, irritability,
confusion  Respiratory collapse leads to unconsciousness and cardiovascular
collapse Collaborative Management 1. Early recognition of respiratory status and
treat cause 2. Restore ventilation and gas exchange; CPR for respiratory failure
with oxygen supplementation; intubation and ventilator support if indicated 3.
Treatment of respiratory infections with bronchodilators, antibiotic therapy 4.
Reverse excess anesthetics and narcotics with medications such as naloxone (Narcan)
5. Chronic respiratory conditions  Breathe in response to low oxygen levels 
Adjusted to high carbon dioxide level through metabolic compensation (therefore,
high CO2 not a breathing trigger)  Cannot receive high levels of oxygen, or will
have no trigger to breathe; will develop carbon dioxide narcosis  Treat with no
higher than 2 liters O2 per cannula 6. Continue respiratory assessments, monitor
further arterial blood gas results

Signs and Symptoms  Compensation: kidneys compensate by eliminating bicarbonate

ions; decrease in bicarbonate HCO3 < 22 mm Hg.  Respiratory: hyperventilating:
shallow, rapid breathing  Neuro: panicked, light-headed, tremors, may develop
tetany, numb hands and feet (related to symptoms of hypocalcemia; with elevated pH
more Ca ions are bound to serum albumin and less ionized “active” calcium available
for nerve and muscle conduction)  May progress to seizures, loss of consciousness
(when normal breathing pattern returns)  Cardiac: palpitations, sensation of chest
tightness Collaborative Management 1. 2. Treatment: encourage client to breathe
slowly in a paper bag to rebreathe CO2 Breathe with the patient; provide emotional
support and reassurance, anti-anxiety agents, sedation On ventilator, adjustment of
ventilation settings (decrease rate and tidal volume) Prevention: pre-procedure
teaching, preventative emotional support, monitor blood gases as indicated

3. 4.

METABOLIC ACIDOSIS  pH <7.35  Deficit of bicarbonate in the blood NaHCO3 <22

mEq/L  Caused by an excess of acid, or loss of bicarbonate from the body Common
Stimuli a. Acute lactic acidosis from tissue hypoxia (lactic acid produced from
anaerobic metabolism with shock, cardiac arrest) b. Ketoacidosis (fatty acids are
released and converted to ketones when fat is used to supply glucose needs as in
uncontrolled Type 1 diabetes or starvation) c. Acute or chronic renal failure
(kidneys unable to regulate electrolytes) d. Excessive bicarbonate loss (severe
diarrhea, intestinal suction, bowel fistulas) e. Usually results from some other
disease and is often accompanied by electrolyte and fluid imbalances f.
Hyperkalemia often occurs as the hydrogen ions enter cells to lower the pH
displacing the intracellular potassium; hypercalcemia and hypomagnesemia may occur
Signs and Symptoms  Compensation: respiratory system begins to compensate by
increasing the depth and rate of respiration in an effort to lower the CO2 in the
blood; this causes a decreased level of carbon dioxide: pCO2 <35 mm HG.  Neuro
changes: headache, weakness, fatigue progressing to confusion, stupor, and coma 
Cardiac: dysrhythmias and possibly cardiac arrest from hyperkalemia  GI: anorexia,
nausea, vomiting  Skin: warm and flushed
Abejo
RESPIRATORY ALKALOSIS  pH < 7.35  pCO2 < 35 mm Hg.  Carbon dioxide deficit,
secondary to hyperventilation Common Stimuli a. Hyperventilation with anxiety from
uncontrolled fear, pain, stress (e.g. women in labor, trauma victims) b. High fever
c. Mechanical ventilation, during anesthesia

MS: Fluids and Electrolyte

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

Respiratory: tries to compensate by hyperventilation: deep and rapid respirations

known as Kussmaul‟s respirations

1. 2. 3. 4.

Diagnostic test findings: 1. ABG: pH < 7.35, HCO3 < 22 2. Electrolytes: Serum K+
>5.0 mEq/L 3. Serum Ca+2 > 10.0 mg/dL 4. Serum Mg+2 < 1.6 mg/dL Collaborative
Management 1. Medications: Correcting underlying cause will often improve acidosis
2. Restore fluid balance, prevent dehydration with IV fluids 3. Correct electrolyte
imbalances 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 acidosis) Be careful not to
overtreat and put client into alkalosis 5. As acidosis improves, hydrogen ions
shift out of cells and potassium moves intracellularly. Hyperkalemia may become
hypokalemia and potassium replacement will be needed. 6. Assessment  Vital signs 
Intake and output  Neuro, GI, and respiratory status;  Cardiac monitoring 
Reassess repeated arterial blood gases and electrolytes

Correcting underlying cause will often improve alkalosis Restore fluid volume and
correct electrolyte imbalances (usually IV NaCl with KCL). With severe cases,
acidifying solution may be administered. Assessment  Vital signs  Neuro, cardiac,
respiratory assessment  Repeat arterial blood gases and electrolytes

Selected Water and Electrolyte Solutions

Isotonic Solutions
A. 0.9% NaCl (isotonic, also called NSS) Na+ 154 mEq/L Cl- 154 mEq/L (308 mOsm/L)
Also available with varying concentrations of dextrose (the most frequent used is a
5% dextrose concentration  An isotonic solution that expands the ECF volume, used
in hypovolemic states, resuscitative efforts, shock, diabetic ketoacidosis,
metabolic alkalosis, hypercalcemia, mild Na deficit Supplies an excess of Na and
Cl; can cause fluid volume excess and hyperchloremic acidosis if used in excessive
volumes, particularly in patients with compromised renal function, heart failure or
edema Not desirable as a routine maintenance solution, as it provides only Na and
Cl (and these are provided in excessive amounts) When mixed with 5% dextrose, the
resulting solution becomes hypertonic in relation to plasma, and in addition to the
above described electrolytes, provides 170cal/L Only solution that may be
administered with blood products

METABOLIC ALKALOSIS  pH >7.45  HCO3 > 26 mEq/L  Caused by a bicarbonate excess,

due to loss of acid, or a bicarbonate excess in the body Common Stimuli a. Loss of
hydrogen and chloride ions through excessive vomiting, gastric suctioning, or
excessive diuretic therapy Response to hypokalemia b. Excess ingestion of
bicarbonate rich antacids or excessive treatment of acidosis with Sodium
Bicarbonate Signs and Symptoms  Compensation: Lungs respond by decreasing the
depth and rate of respiration in effort to retain carbon dioxide and lower pH 
Neuro: altered mental status, numbness and tingling around mouth, fingers, toes,
dizziness, muscle spasms (similar to hypocalcemia due to less ionized calcium
levels)  Respiratory: shallow, slow breathing Diagnostic test findings 1. ABG‟s:
pH> 7.45, HCO3 >26 2. Electrolytes: Serum K+ < 3.5 mEq/L 3. Electrocardiogram: as
with hypokalemia

 


B. Lactated Ringer’s solution (Hartmann’s solution) Na+ 130 mEq/L K+ 4 mEq/L Ca++ 3
mEq/L Cl- 109 mEq/L Lactate (metabolized to bicarbonate) 28 mEq/L (274 mOsm/L) Also
available with varying concentration of dextrose (the most common is 5% dextrose)
 An isotonic solution that contains multiple electrolytes in roughly the same
concentration as found in plasma (note that solution is lacking in Mg++) provides 9
cal/L Used in the tx of hypovolemia, burns, fluid lost as 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 disorder.
Abejo

 

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

  

Not to be given with a pH > 7.5 because bicarbonates is formed as lactate breaks
down causing alkalosis Should not be used in renal failure because it contains
potassium and can cause hyperkalemia Similar to plasma

Hypertonic Solutions
E. 3% NaCl (hypertonic saline) Na+ 513 mEq/L Cl- 513 mEq/L (1026 mOsm/L)     
Used to increase ECF volume, decrease cellular swelling Highly hypertonic solution
used only in critical situations to treat hyponatremia Must be administered slowly
and cautiously, because it can cause intravascular volume overload and pulmonary
edema Supplies no calories Assists in removing ICF excess

C. 5% Dextrose in Water (D5W) No electrolytes 50 g of glucose          An

isotonic solution that supplies 170 cal/L and free water to aid in renal excretion
of solutes Used in treatment of hypernatremia, fluid loss and dehydration Should
not be used in excessive volumes in the early post-op period (when ADH secretion is
increased due to stress reaction) Should not be used solely in tx of fluid volume
deficit, because it dilutes plasma electrolyte concentrations Contraindicated in
head injury because it may cause increased intracranial pressure Should not be used
for fluid resuscitation because it can cause hyperglycemia Should be used with
caution in patients with renal or cardiac dse because of risk of fluid overload
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 metabolized by body. Overtime D5W without NaCl can cause water
intoxication (ICF vol. excess bec. solution is hypotonic)

F. 5% NaCl (hypertonic solution) Na+ 855 mEq/L Cl- 855 mEq/L (1710 mOsm/L)   
Highly hypertonic solution used to treat symptomatic hyponatremia Administered
slowly and cautiously, because it can cause intravascular volume overload and
pulmonary edema Supplies no calories

Colloid Solutions
G. Dextran in NS or 5% D5W Available in low-molecular-weight (Dextran 40) and
highmolecular-weight (Dextran 70) forms   Colloid solution used as volume/plasma
expander for intravascular part of ECF Affects clotting by coating platelets and
decreasing ability to clot Remains in circulatory system up to 24 hours Used to
treat hypovolemia in early shock to increase pulse pressure, CO, and arterial BP
Improves microcirculation by decreasing RBC aggregation Contraindicated in
hemorrhage, thrombocytopenia, renal dse and severe dehydration Not a substitute for
blood or blood products

Hypotonic Solutions
D. 0.45% NaCl half-strength saline) Na+ 77 mEq/L Cl- 77 mEq/L (154 mOsm/L) Also
available with varying concentration of dextrose (the most common is 5% dextrose) 
   Provides Na, Cl and free water Free water is desirable to aid the kidneys in
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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MS: Fluids and Electrolyte

Abejo