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

Lecturer: Mark Fredderick R. Abejo RN, MAN

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

B. Locations of ECF:
1. Interstitial: fluid between most cells Hydrostatic pressure -pushes fluid out of vessels into tissue
2. Intravascular: fluid within blood space; higher to lower pressure
vessels; also called plasma – due to water volume in vessels; greater in arterial end
3. Transcellular: fluids of body – swelling: varicose veins, fluid overload, kidney failure
including urine, digestive secretion, & CHF
cerebrospinal, pleural, synovial, Osmotic pressure -pulls fluid into vessels; from weaker
intraocular, gonadal, pericardial 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

4. Angiotensin II = vasoconstriction & aldosterone

V. Mechanisms that Regulate Homeostasis: release
How the body adapts to fluid and electrolyte changes?
ADH – produced by hypothalamus, released by posterior
A. Thirst: primary regulator of water intake pituitary when osmoreceptor or baroreceptor is
(thirst center in brain) triggered in hypothalamus
B. Kidneys: regulator of volume and
osmolality by controlling excretion of water Aldosterone – produced by adrenal cortex; promotes Na &
and electrolytes water reabsorption
C. Renin-angiotension-aldosterone
mechanism: response to a drop in blood
pressure; results from vasoconstriction and Sensible & Insensible Fluid Loss
sodium regulation by aldosterone
D. Antidiuretic hormone: hormone to Sensible: urine, vomiting, suctioned secretions
regulate water excretion; responds to Insensible: lungs , skin, GI and evaporation
osmolality and blood volume
E. Atrial natriuretic factor: hormone from
atrial heart muscle in response to fluid Normal Fluid Intake and Loss in Adults
excess; causes increased urine output by
blocking aldosterone Intake:
 Water in food 1,000 mls
Fluid Balance Regulation  Water from oxidation 300 mls
 Water in liquid 1,200 mls
Thirst reflex triggered by:
1. decreased salivation & dry mouth TOTAL 2,500 mls
2. increased osmotic pressure stimulates
osmoreceptors in the hypothalamus Output:
3. decreased blood volume activates the  Skin 500 mls
renin/angiontensin pathway, which simulates the  Lungs 300 mls
thirst center in hypothalamus  Feces 150 mls
 Kidneys 1,500 mls
Renin-Angiotensin TOTAL 2,500 mls
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

MS: Fluids and Electrolyte Abejo

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

IV Fluids d. Hemorrhage
Isotonic LR e. Coma
PNSS (0.9%NSS) f. Third-spacing conditions like ascites,
NM pancreatitis and burns

Hypotonic D5W
- isotonic in bag PATHOPHYSIOLOGY:
- dextrose=quickly
metabolized=hypotonic Risk Factors --- inadequate fluids in the body ---- decreased
D2.5W blood volume ----- decreased cellular hydration ---- cellular
0.45% NSS shrinkage ---- weight loss, decreased turgor, oliguria,
0.3% NSS
hypotension, weak pulse, etc.
0.2% NSS

Hypertonic D50W
D10W ASSESSMENT:
D5NSS
D5LR Physical examination
3%NSS
 Weight loss, tented skin turgor, dry mucus membrane
Colloids (usually CHONs) & Plasma expanders  Hypotension
 Tachycardia
Dextran – synthetic polysaccharide, glucose solution  Cool skin, acute weight loss
- increase concentration of blood, improving blood  Flat neck veins
volume up to 24 hrs  Decreased CVP
- contraindicated: heart failure, pulmonary edema,
cardiogenic shock, and renal failure Subjective cues
Hetastarch – like Dextran, but longer-acting  Thirst
- expensive  Nausea, anorexia
- derived from corn starch  Muscle weakness and cramps
 Change in mental state
Composition of Fluids

Saline solutions – water, Na, Cl Laboratory findings

Dextrose solutions – water or saline, calories 1. Elevated BUN due to depletion of fluids or decreased
Lactated Ringer‟s – water, Na, Cl, K, Ca, lactate renal perfusion
Plasma expanders – albumin, dextran, plasma protein 2. Hemoconcentration
(plasmanate) - increases oncotic pressure, pulling fluids 3. Possible Electrolyte imbalances: Hypokalemia,
into circulation Hyperkalemia, Hyponatremia, hypernatremia
Parenteral hyperalimentation – fluid, electrolytes, amino 4. Urine specific gravity is increased (concentrated
acids, calories urine) above 1.020

A. FLUID VOLUME DEFICIT or HYPOVOLEMIA NURSING MANAGEMENT

 Definition: This is the loss of extra cellular fluid 1. Assess the ongoing status of the patient by doing an
volume that exceeds the intake of fluid. The loss of accurate input and output monitoring
water and electrolyte is in equal proportion. It can 2. Monitor daily weights. Approximate weight loss 1
be called in various terms- vascular, cellular or kilogram = 1liter!
intracellular dehydration. But the preferred term is 3. Monitor Vital signs, skin and tongue turgor, urinary
hypovolemia. concentration, mental function and peripheral
 Dehydration refers to loss of WATER alone, with circulation
increased solutes concentration and sodium 4. Prevent Fluid Volume Deficit from occurring by
concentration identifying risk patients and implement fluid
replacement therapy as needed promptly
Pathophysiology of Fluid Volume Deficit 5. Correct fluid Volume Deficit by offering fluids orally
if tolerated, anti-emetics if with vomiting, and foods
 Etiologic conditions include: with adequate electrolytes
a. Vomiting 6. Maintain skin integrity
b. Diarrhea 7. Provide frequent oral care
c. Prolonged GI suctioning 8. Teach patient to change position slowly to avoid
d. Increased sweating sudden postural hypotension
e. Inability to gain access to fluids
f. Inadequate fluid intake
g. Massive third spacing B. FLUID VOLUME EXCESS: HYPERVOLEMIA
 Definition : Refers to the isotonic expansion of
 Risk factors are the following: the ECF caused by the abnormal retention of
a. Diabetes Insipidus water and sodium
b. Adrenal insufficiency
c. Osmotic diuresis
MS: Fluids and Electrolyte Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

 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
4. Teach patient about edema, ascites, and fluid therapy.
Advise elevation of the extremities, restriction of
fluids, necessity of paracentesis, dialysis and diuretic
therapy.

MS: Fluids and Electrolyte Abejo

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

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 EXCESS: HYPERNATREMIA
sodium levels have more severe symptoms and higher
mortality rates than do those with more slowly  Serum Sodium level is higher than 145 mEq/L
developing hyponatremia.  There is a gain of sodium in excess of water or a
 Features of hyponatremia associated with sodium loss loss of water in excess of sodium.
and water gain include anorexia, muscle cramps, and a
feeling of exhaustion. Pathophysiology:
 When the serum sodium level drops below 115 mEq/L
(SI: 115 mmol/L), thee ff signs of increasing Etiologic factors
intracranial pressure occurs: a. Fluid deprivation
 lethargy b. Water loss from Watery diarrhea, fever, and
 Confusion hyperventilation
 muscular twitching c. Administration of hypertonic solution
 focal weakness d. Increased insensible water loss
 hemiparesis e. Inadequate water replacement, inability to swallow
 papilledema f. Seawater ingestion or excessive oral ingestion of salts
 convulsions

MS: Fluids and Electrolyte Abejo

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

3. Urine specific gravity and osmolality INCREASED

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

Laboratory findings 6. Regulations: renal secretion and excretion,

1. Serum sodium level exceeds 145 mEq/L * Aldosterone promotes renal excretion
2. Serum osmolality exceeds 295 mOsm/kg * Acidosis promotes K exchange for hydrogen

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

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

The Nursing Process in Hyperkalemia

Potassium Excess (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
peripheral neuromuscular system, it has little effect on NURSING MANAGEMENT
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
ASSESSMENT monitored and that the potassium supplement is given
Physical Examination correctly
 Diarrhea 6. Assist in hemodialysis if hyperkalemia cannot be
 Skeletal muscle weakness corrected.
 Abnormal cardiac rate 7. Provide client teaching. Advise patients at risk to avoid
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:

1. Needed for formation of bones and teeth

2. For muscular contraction and relaxation
3. For neuronal and cardiac function
MS: Fluids and Electrolyte Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

4. For enzymatic activation

5. For normal blood clotting  Clinical Manifestation
 Decreased cardiac contractility
Regulations:  Arrhythmia
 ECG: prolonged QT interval, lengthened ST
1. GIT- absorbs Ca+ in the intestine; Vitamin D helps to segment
increase absorption  Trousseau’s sign (inflate BP cuff 20mm above
2. Renal regulation- Ca+ is filtered in the glomerulus systole for 3 min = carpopedal spasm)
and reabsorbed in the tubules:
3. 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
 Chvostek’s sign (tap facial nerve anterior to the
deposition of calcium in the bones.
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: HYPERCALCEMIA
milk, yogurt, cheese, sardines, broccoli, tofu, green leafy
vegetables  is an elevated calcium level in the blood
 usually from bone resorption
HYPOCALCEMIA
 Low levels of calcium in the blood  Risk Factors / Causes
a. Hyperparathyroidism (eg adenoma)
 Risk Factors b. Metastatic cancer (bone resorption as tumor‟s
a. Hypoparathyroidism (idiopathic or postsurgical) ectopic PTH effect) – eg. Multiple myeloma
b. Alkalosis (Ca binds to albumin) c. Thiazide diuretics (potentiate PTH effect)
c. Corticosteroids (antagonize Vit D) d. Immobility
d. Hyperphosphatemia e. Milk-alkali syndrome (too much milk or antacids
e. Vit D deficiency in aegs with peptic ulcer)
f. Renal failure (vit D deficiency)
MS: Fluids and Electrolyte Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

 Clinical Manifestation h. Excess calcium

 groans (constipation) i. Excess saturated fats
 moans (psychotic noise) j. Excess coffee or tea intake
 bones (bone pain, especially if PTH is elevated) k. Excess phosphoric or carbonic acids (soda pop)
 stones (kidney stones) l. Insufficient water consumption
 psychiatric overtones (including depression and m. Excess salt or sugar intake
confusion) n. Insufficient selenium,vitamin D, sunlight
exposure or vitamin B6
 Arrhythmia o. Increased levels of stress
 ECG: shortened QT interval, decreased ST
segment  Clinical Manifestation
 Hyporeflexia, lethargy, coma  Weakness
 muscle cramps
Collaborative Management  cardiac arrhythmia
1. If parathyroid tumor = surgery  increased irritability of the nervous system with
2. Diet: low Ca, stop taking Ca Carbonate antacids, tremors, athetosis, jerking, nystagmus and an
increase fluids extensor plantar reflex. Confusion
3. IV flushing (usually NaCl)  disorientation
4. Loop diuretics  hallucinations
5. Corticosteroids  depression
6. Biphosphonates, like etidronate (Calcitonin) &  epileptic fits
alendronate (Fosamax)  hypertension, tachycardia and tetany.
7. Plicamycin (Mithracin) – inhibits bone resorption
8. Calcitonin – IM or intranasal * Like hypocalcemia, hypokalemia
9. Dialysis (severe case) Potentiates digitalis toxicity
10. Watch out for digitalis toxicity
11. Prevent fractures, handle gently Collaborative Management
1. Magnesium sulfate IV, IM (make sure renal
function is ok) – may cause flushing
MAGNESIUM 2. Oral: Magnesium oxide 300mg/day,
3. Mg-containing antacids (SE diarrhea)
4. Diet: high magnesium (fruits,green vegetables,
 2nd most abundant intracellular cation whole grains cereals, milk, meat, nuts and sea
 50% found in bone, 45% is intracellular foods )
 ATP (adenosine triphosphate), the main source of 5. Promotion of safety, protect from injury
energy in cells, must be bound to a magnesium ion in
order to be biologically active.
 competes with Ca & P absorption in the GI HYPERMAGNESEMIA
 inhibits PTH
 Normal value : 1.5-2.5 mEq/L  Etiologic Factors
a. Magnesium treatment for pre-eclampsia
Functions: b. Renal failure
1. important in maintaining intracellular activity c. Diabetic Ketoacidosis
2. affects muscle contraction, & especially relaxation d. Excessive use of Mg antacids/laxatives
3. maintains normal heart rhythm
4. promotes vasodilation of peripheral arterioles
PATHOPHYSIOLOGY
Sources: Increase Mg. ----- Blocks acetylcholine release ---- decrease
green leafy vegetables, nuts, legumes, seafood, whole excitability of muscle
grains, bananas, oranges, cocoa, chocolate

HYPOMAGNESEMIA  Clinical Manifestation

 Hyporeflexia
 is an electrolyte disturbance in which there is an  Hypotension, bradycardia, arrhythmia
abnormally low level of magnesium in the blood.  Flushing
 Weakness, lethargy, coma
 Risk Factors and Cause  Decreased RR & respiratory paralysis
a. Chronic alcoholism (most common), Alcohol  Loss of DTR‟s
stimulates renal excretion of magnesium,
b. Inflammatory bowel disease *like hypercalcemia
c. Small bowel resection
d. GI cancer Collaborative Management
e. chronic pancreatitis (poor absorption) 1. Diuretics
f. Loop and thiazide diuretic use (the most common 2. Stop Mg-containing antacids & enemas
cause of hypomagnesemia) 3. IV fluids rehydration
g. Antibiotics (i.e. aminoglycoside, amphotericin, 4. Calcium gluconate – (antidote, antagonizes
pentamidine, gentamicin, tobramycin, viomycin) cardiac & respiratory effects of Mg)
block resorption in the loop of Henle. 5. Dialysis – if RF

MS: Fluids and Electrolyte Abejo

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

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

HYPERPHOSPHATEMIA  Clinical Manifestation

 Deep, rapid respirations (met. Acidosis)
 Risk Factors  hyperK, hyperNa S/S
a. Acidosis (Ph moves out of cell)  Increased Cl sweat levels in cystic fibrosis
b. Cytotoxic agents/chemotherapy in cancer
c. Renal failure
d. Hypocalcemia Collaborative Management
e. Massive BT (P leaks out of cells during storage of 1. Diuretics
blood) 2. Hypotonic solutions, D5W to restore balance
f. Hyperthyroidism 3. Diet: low Cl (& usually Na)
4. Treat acidosis
 Clinical Manifestation
 Calcification of kidney, cornea, heart
 Muscle spasms, tetany, hyperreflexia

*like hypocalcemia

MS: Fluids and Electrolyte Abejo

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

 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
Acid-Base Balance Mechanisms respiratory imbalance
 If it does not reflect an opposite response as the
pH - move to step III
Buffer - prevents major changes in ECF by releasing or
Step 3
accepting H ions
 Look at the HCO3
 Does the HCO3 reflect a corresponding
Buffer mechanism: first line (takes seconds)
 response with the pH
1. combine with very strong acids or bases to
 If it does then the condition is a metabolic
convert them into weaker acids or bases
imbalance
2. Bicarbonate Buffer System
- most important
- uses HCO3 & carbonic acid/H2CO3 - (20:1)
- closely linked with respiratory & renal FACTORS AFFECTING BODY FLUIDS,
mechanisms ELECTROLYTES AND ACID-BASE BALANCE
3. Phosphate Buffer System
- more important in intracellular fluids, where AGE
concentration is higher  Infants have higher proportion of body water than
- similar to bicarbonate buffer system, only uses adults
phosphate  Water content of the body decreases with age
4. Protein Buffer System  Infants have higher fluid turn-over due to immature
- hemoglobin, a protein buffer, promotes kidney and rapid respiratory rate
movement of chloride across RBC membrane in
exchange for HCO3
GENDER AND BODY SIZE
Respiratory mechanism: 2nd line (takes minutes)  Women have higher body fat content but lesser
1. increased respirations liberates more CO2 = water content
increase pH  Lean body has higher water content
2. decreased respirations conserve more CO2 =
decrease pH ENVIRONMENT AND TEMPERATURE
carbonic acid (H2CO3) = CO2 + water  Climate and heat and humidity affect fluid balance

Renal mechanism: 3rd line (takes hours-days)

1. kidneys secrete H ions & reabsorb bicarbonate ions = DIET AND LIFESTYLE
increase blood pH  Anorexia nervosa will lead to nutritional depletion
2. kidneys form ammonia that combines with H ions to  Stressful situations will increase metabolism,
form ammonium ions, which are excreted in the urine increase ADH causing water retention and
in exchange for sodium ions increased blood volume
 Chronic Alcohol consumption causes malnutrition
Review: Acid-Base Imbalance
ILLNESS
pH – 7.35-7.45  Trauma and burns release K+ in the blood
pCO2 – measurement of the CO2 pressure that is being  Cardiac dysfunction will lead to edema and
exerted on the plasma congestion
- 35-45mmHg
PaO2- amount of pressure exerted by O2 on the plasma
- 80-100mmHg MEDICAL TREATMENT, MEDICATIONS AND
SaO2- percent of hemoglobin saturated with O2 SURGERY
Base excess – amount of HCO3 available in the ECF  Suctioning, diuretics and laxatives may cause
- -3 to +3 imbalances

Interpretation Arterial Blood Gases

 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

Step 1
 Look at the pH
 Is it up or down?
 If it is up - it reflects alkalosis
 If it is down - it reflects acidosis

Step 2
MS: Fluids and Electrolyte Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

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

MS: Fluids and Electrolyte Abejo

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

 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
Collaborative Management
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.
MS: Fluids and Electrolyte Abejo
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 Hypertonic Solutions
causing alkalosis
 Should not be used in renal failure because it E. 3% NaCl (hypertonic saline)
contains potassium and can cause hyperkalemia Na+ 513 mEq/L
 Similar to plasma Cl- 513 mEq/L
(1026 mOsm/L)
C. 5% Dextrose in Water (D5W)  Used to increase ECF volume, decrease cellular
No electrolytes swelling
50 g of glucose  Highly hypertonic solution used only in critical
situations to treat hyponatremia
 An isotonic solution that supplies 170 cal/L and  Must be administered slowly and cautiously,
free water to aid in renal excretion of solutes because it can cause intravascular volume
 Used in treatment of hypernatremia, fluid loss and overload and pulmonary edema
dehydration  Supplies no calories
 Should not be used in excessive volumes in the  Assists in removing ICF excess
early post-op period (when ADH secretion is
increased due to stress reaction) F. 5% NaCl (hypertonic solution)
 Should not be used solely in tx of fluid volume Na+ 855 mEq/L
deficit, because it dilutes plasma electrolyte Cl- 855 mEq/L
concentrations (1710 mOsm/L)
 Contraindicated in head injury because it may
cause increased intracranial pressure  Highly hypertonic solution used to treat
 Should not be used for fluid resuscitation because symptomatic hyponatremia
it can cause hyperglycemia  Administered slowly and cautiously, because it
 Should be used with caution in patients with renal can cause intravascular volume overload and
or cardiac dse because of risk of fluid overload pulmonary edema
 Electrolyte-free solutions may cause peripheral  Supplies no calories
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 Colloid Solutions
NaCl can cause water intoxication (ICF vol.
excess bec. solution is hypotonic) G. Dextran in NS or 5% D5W
Available in low-molecular-weight (Dextran 40) and high-
molecular-weight (Dextran 70) forms

Hypotonic Solutions  Colloid solution used as volume/plasma expander

for intravascular part of ECF
D. 0.45% NaCl  Affects clotting by coating platelets and
half-strength saline) decreasing ability to clot
Na+ 77 mEq/L  Remains in circulatory system up to 24 hours
Cl- 77 mEq/L  Used to treat hypovolemia in early shock to
(154 mOsm/L) increase pulse pressure, CO, and arterial BP
Also available with varying concentration of dextrose (the  Improves microcirculation by decreasing RBC
most common is 5% dextrose) aggregation
 Contraindicated in hemorrhage,
 Provides Na, Cl and free water thrombocytopenia, renal dse and severe
 Free water is desirable to aid the kidneys in dehydration
elimination of solute  Not a substitute for blood or blood products
 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

MS: Fluids and Electrolyte Abejo