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Fluids and Electrolytes
Water, water everywhere… but not a drop to drink…

WALT WHITMAN

FLUID BALANCE
Water and its electrolytes are distributed in two major compartments:
63% of the total body water is found within cells across the age groups.
37% of the total body water is found outside the cells, mainly in tissue spaces, plasma of blood,
and lymph.
The intracellular and extracellular fluid compartments are maintained in a steady state to ensure
proper physiologic functioning.
Water and its electrolytes are distributed in two major compartments:
63% of the total body water is found within cells across the age groups.
37% of the total body water is found outside the cells, mainly in tissue spaces, plasma of blood,
and lymph.
The intracellular and extracellular fluid compartments are maintained in a steady state to ensure
proper physiologic functioning.
TOTAL BODY WATER
(AS PERCENTAGE OF BODY WEIGHT)
IN RELATION TO AGE AND SEX
AGE MALE FEMALE
UNDER 18 65% 55%
18-40 60% 50%
40-60 50-60% 40-50%
OVER 60 50% 40%

Intracellular Fluid Compartment

Includes all the water and electrolytes inside the cells of the body.
Approximately 63% of the total body water is contained within cell membranes.
Contains high concentrations of potassium, phosphate, magnesium and sulfate ions, along with
most of the proteins in the body.
EXAMPLE: How much water is in the intracellular fluid compartment of a 25-year old male patient
who weighs 60 kg?

Step #1: Compute the total body water (TBW) based on age and sex.
TBW = (60 kg) (0.6)
= 36 kg  weight of water
= 36 liters  volume of water
Step #2: Compute for the intracellular fluid volume (usually 63% of the total body water is
intracellular fluid)
ICF = (36 liters) (0.63)
= 22.7 liters

Extracellular Fluid Compartment

Includes all the fluid outside the cells: interstitial fluid, plasma, lymph, secretions of glands, fluid
within subcompartments separated by epithelial membranes.
Constitutes approximately 37% of the total body water.

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Contains high concentrations of sodium, chloride and bicarbonate.
One-third of the ECF is in plasma.

EXAMPLE: How much water is in the circulatory system of a 32-year old female patient who
weighs 52 kg?
Step #1: Compute for the total body water based on age and sex.
TBW = (52 kg) (0.5)
= 26 kg  weight of water
= 26 liters  volume of water
Step #2: Compute for the extracellular fluid volume (usually 37% of the total body water).
ECF = (26 liters) (0.37)
= 9.6 liters

Step #3: Compute for the plasma volume.

Plasma = (9.6 liters)/3
= 3.2 liters
Transcellular Exchange Mechanisms:
ACTIVE TRANSPORT
PASSIVE TRANSPORT
Diffusion
Osmosis
Filtration
Facilitated diffusion

Serum Osmolality
Reflects the amount of solute particles in a solution and is a measure of the concentration of a
given solution.
Can be calculated using the formula:
Osmserum = 2 (Na) + BUN + glucose
Normal value = 285 – 295 mosm/kg
Sodium is the most active determinant of serum osmolality and is therefore actively moved
across membranes to ensure normal osmolality.

Hence, if too much salt is used in food, the pulse hardens.

HUANG TI (THE YELLOW EMPEROR), 2697-2597 B.C.

Ions

NORMAL VALUES AND MASS CONVERSION FACTORS

Normal Plasma Mass
Values Conversion
Sodium (Na+) 135 – 145 meq/L 23 mg = 1 meq
Potassium (K+) 3.5 – 5.0 meq/L 39 mg = 1 meq
Chloride (Cl-) 98 – 107 meq/L 35 mg = 1 meq
Bicarbonate (HCO3-) 22 – 26 meq/L 61 mg = 1 meq
Calcium (Ca2+) 8.5 – 10.5 mg/dL 40 mg = 1 mmol
Phosphorus 2.5 – 4.5 mg/dL 31 mg = 1 mmol
Magnesium (Mg2+) 1.8 – 3.0 mg/dL 24 mg = 1 mmol
Osmolality 285 – 295 mosm/kg -
265 - 305 mosm/kg

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Sodium
Dominant extracellular ion.
About 90 to 95% of the osmotic pressure of the extracellular fluid results from sodium ions and
the negative ions associated with them.
Recommended dietary intake is less than 2.5 grams per day.
Kidneys provide the major route by which the excess sodium ions are excreted.
Sodium
In the presence of aldosterone, the reabsorption of sodium ions in the loop of Henle is very
efficient. When aldosterone is absent, the reabsorption of sodium in the nephron is greatly
reduced and the amount of sodium lost in the urine increases.
Also excreted from the body through the sweat mechanism.
Primary mechanisms that regulate the sodium ion concentration in the extracellular fluid:
Changes in the blood pressure
Changes in the osmolality of the extracellular fluid

Sodium Regulation
Increased ADH secretion, Decreased urine
INCREASED volume and increased plasma volume
SODIUM
Decreased aldosterone secretion, DECREASED
decreased sodium reabsorption SODIUM

NORMAL Na+

Decreased ADH secretion, Increased

DECREASED urine volume and decreased plasma
SODIUM INCREASED
volume
SODIUM
Increased aldosterone secretion,
increased sodium reabsorption

Potassium
Electrically excitable tissue such as muscle and nerves are highly sensitive to slight changes in
extracellular potassium concentration.
The ECF concentration of potassium must be maintained within a narrow range for tissues to
function normally.
Aldosterone also plays a major role in regulating the concentration of potassium ions in the ECF.
Circulatory system shock resulting from plasma loss, dehydration, and tissue damage causes
extracellular potassium ions to become more concentrated than normal. In response, aldosterone
secretion increases and causes potassium secretion to increase.
Potassium regulation

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Increased aldosterone secretion with

increased potassium secretion by the
INCREASED
kidneys and increased potassium in urine DECREASED
POTASSIUM
POTASSIUM

NORMAL K+

DECREASED
POTASSIUM Decreased aldosterone secretion with INCREASED
decreased potassium secretion by the POTASSIUM
kidney and decreased potassium in the
urine

Calcium
Extracellular concentration of calcium ions is maintained within a narrow range.
Increases and decreases in ECF concentration of calcium ions have dramatic effects on the
electrical properties of excitable tissues.
Parathyroid hormone (PTH) secreted by the parathyroid glands increases extracellular calcium
levels.
Calcitonin is secreted by the thyroid gland.
It reduces blood levels of calcium when they are too high.
Calcium Regulation
Increased Calcitonin secretion with
decreased bone resorption

INCREASED Decreased parathyroid hormone

CALCIUM secretion with decreased bone DECREASED
resorption, decreased intestinal CALCIUM
calcium absorption, and decreased
kidney calcium reabsorption

NORMAL Ca++
INCREASEDCAL
CIUM
DECREASED
CALCIUM Increased parathyroid hormone secretion with
increased bone resorption, increased intestinal
calcium absorption, and increased renal calcium
reabsorption

Phosphate and Sulfate

Phosphate and sulfate are reabsorbed by active transport in the kidneys.
Rate of reabsorption is slow, so that if the concentration of these ions in the filtrate exceeds the
ability of the nephron to reabsorb them, the excess is excreted in the urine.

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Fluid and Electrolyte Management

General Management of Fluids
Maintenance Therapy:
Minimum Water Requirements
Can be estimated from the sum of the urine output necessary to excrete the daily solute load
(500 mL per day if the urine concentrating ability is normal) plus the insensible water losses from
the skin and respiratory system (500 to 1000 mL per day), minus the amount of water produced
from endogenous metabolism (300 mL per day)
Two to three liters of water are needed to produce a urine volume of 1 to 1.5 liters daily.

Fluid / Electrolyte Replacement:

Insensible Water Losses
Usually average 500 to 1000 mL daily, and depend on respiratory rate, ambient temperature,
humidity and body temperature.
Water losses increase by 100 ml daily for each degree of body temperature over 37°C.
Fluid losses from sweating can vary enormously and depend on physical activity and body and
ambient temperature.
Mechanical ventilation accentuate losses from the respiratory tract.
A 72-year old female was admitted for pneumonia in the elderly, community-acquired.

Previous day’s profile:

Total urine output: 1,700 ml
3 episodes of loose stools, approximately 250 per episode
Highest temperature: 39.7 degrees Celsius
On mechanical ventilator for the past three days
Today’s Orders:
NGT feeding with the following:
TCR: 1700 kcal/day
6 equal feedings, 2:1 dilution
Flush with 100 ml plain water after every feeding

Compute for the IVF rate for today if the patient is to be connected to an adult venoset.
What would be your choice of IVF?
Maintenance Therapy:
Minimum Water Requirements
Weighing the patient daily is the best means of assessing net gain or loss of fluid, since the
gastrointestinal, renal and insensible fluid losses of the hospitalized patient are unpredictable.

ECF Volume Depletion

Occurs with losses of both sodium and water.
The character of the fluid loss will dictate the clinical picture. If the loss is isotonic, the
osmolality is unaffected and intracellular volume will change minimally.
Loss of hypotonic fluid will lead to an increase in serum or plasma osmolality.

ECF Volume Depletion

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TYPE OTHER NAME RESULTING SERUM
OSMOLALITY
Hypotonic volume loss Hypertonic or Elevated serum
hyperosmolar osmolality
dehydration
Hypertonic volume loss Hypotonic or Decreased serum
hypoosmolar osmolality
dehydration
Isotonic volume loss Isotoniic or Normal serum
normoosmolar osmolality
dehydration

TYPE CLASSIC EXAMPLES MANAGEMENT

Hypotonic volume loss Diabetes insipidus Hypotonic fluid

(predominant water replacement
loss)
Hypertonic volume loss Burns, Nephrotic Hypertonic fluid
syndrome replacement
Isotonic volume loss Most usual types of Isotonic fluid
dehydration replacement
(gastrointestinal (goal: restore volume)
losses, etc.)
Manifestations of ECF volume depletion depend on the magnitude and on serum
osmolality.

Symptoms:

Anorexia
Nausea
Vomiting
Apathy
Weakness
Orthostatic lightheadedness
Syncope
Weight loss is an important sign and provides an estimate of the magnitude of the volume
deficit.
Other physical findings:
Orthostatic hypotension
Poor skin turgor
Sunken eyes
Absence of axillary sweat
Oliguria
Tachycardia
Shock and coma (severe volume depletion)

ECF Volume Depletion: Treatment

Should be directed at restoration of the ECF volume with solutions containing the lost water and
electrolytes.
Daily assessment of weight, ongoing fluid losses and serum electrolyte concentrations.
Mild degrees of volume depletion can be corrected orally.

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More severe deficits accompanied by circulatory compromise should be treated initially through
intravenous isotonic fluid replacement until hemodynamic stability has been restored. One to two
liters of fluid should be given over the first hour.

Parenteral Solutions

Further therapy should be guided by the symptoms and signs.

Used in reference to fluids administered via extra-enteric routes, usually intravenous.
May either be colloidal solutions or crystalline solutions.

Parenteral Osmolality Contents Indications

Solution
Colloidal May be isotonic, Water and Hypertonic
solutions although most are organic solutes volume loss,
hypertonic parenteral
nutrition,
volume
expanders
Crystalloids Variable, depending Water and Volume
on the electrolyte mostly replacement
contents electrolytes

Parenteral Solutions
(Crystalloids)
COMMONLY USED PARENTERAL SOLUTIONS
IV Solutions Osmolality Glucose Sodium Chloride
(mosm/kg) (g/liter) (meq/liter) (meq/liter)
5% D/W 252 50 - -
10% D/W 505 100 - -
50% D/W 2525 500 - -
0.45% NaCl 154 - 77 77
0.9% NaCl 308 - 154 154
3% NaCl 1026 - 513 513
Ringer’s 282 - 130 109
lactate
5% D/NR 294 50 147 147
5% D/NM 290 50 77 77
ECF Volume Excess
Manifestations:
Weight gain is the most sensitive and consistent sign of ECF volume excess.
Edema is usually not apparent until 2 to 4 kg of fluid have been retained.
Dyspnea
Tachycardia
Jugular venous distention
Hepatojugular reflux
Rales on pulmonary auscultation
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Causes:
Heart, liver or renal failure
Excessive renal sodium and water retention
Unnecessary salt administration

Treatment
Must address not only the ECF volume excess but also the underlying pathologic process.
Treatment of the nephrotic syndrome and the cardiovascular volume overload associated with
renal failure.
Treatment of heart failure and cirrhosis

.
Fluid and Electrolyte Management
Sodium
The primary extracellular cation.
Always accompanies water in the extracellular fluid compartment.
Hyponatremia
Defined as serum concentration less than 135 meq/L.
Most common electrolyte abnormality observed in a general hospitalized population.
Initial approach is the determination of serum osmolality.

Hyponatremia

SERUM OSMOLALITY

Normal Low High

ISOTONIC HYPERTONIC
Hyponatremia HYPOTONIC Hyponatremia
Hyperproteinemia Hyponatremia
Hyperglycemia
Hyperlipidemia Mannitol, sorbitol,
Glycerol, maltose
VOLUME STATUS

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Hyponatremia
VOLUME STATUS

Hypovolemic Hypervolemic
Euvolemic
Una <10 meq/L
U >20 meq/L SIADH Edematous states:
Extrarenal salt na
Renal salt loss Postop HypoNa Congestive heart failure
Dehydration Hypothyroidism
Diuretics Hepatic disease
Diarrhea Psychogenic
ACE-inhibitors Nephrotic syndrome
Vomiting Nephropathies polydipsia Advanced CHF
Mineralo- Beer potomania
Corticoid lack Drug reactions

Treatment
Hypertonic (3%) saline with furosemide is indicated for symptomatic hyponatremic patients.
For asymptomatic patients, approach includes water restriction, isotonic saline infusion and
administration of demeclocycline.
Hypernatremia
Serum sodium > 145 meq/L
Develops from excess water loss, frequently accompanied by an impaired thirst mechanism.
Hypernatremia: Treatment
Directed toward correcting the cause of the fluid loss and replacing water and, as needed,
electrolytes.
Calculation of water deficit:
When calculating fluid replacement, both the deficit and the maintenance requirement should be
added to each 24-hour replacement regimen.

Calculation of water deficit (cont’d)

Water deficit = current TBW x ([Na] – 140)
140
where [Na] is the measured serum sodium and
TBW is the total body water (as percentage of the total body weight based on age and
sex.
 Given a 38/F with a body weight of 50 kg and a serum sodium level of 160 meq/L:
What is the total water deficit?
How much water should you give your patient during the first 24 hours?
Hypernatremia: Treatment
Water deficit = TBW x ([Na] - 140)
140
= (50 kg)(0.5) (160-140)
140
= 25 liters (20)
140
= 25 liters (0.14)
= 3.5 liters
Volume to be replaced in 24 hours =
TBW x (160 – 148)
148
= 25 liters (12)
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148
= 25 liters (0.08)
= 2 liters

Fluid and Electrolyte Management

Potassium

Hypokalemia
A total body deficit of about 350 meq occurs for each 1 meq/L decrement in serum potassium
concentration.
Changes in blood pH and hormones (insulin, aldosterone, and β-adrenergic agonists)
independently affect serum potassium levels.
Hypokalemia: Clinical Findings
Symptoms and Signs:
Muscular weakness
Fatigue
Muscle cramps
Constipation or ileus
Flaccid paralysis, hyporeflexia, and rhabdomyolysis

Laboratory Findings:
Decreased amplitude and broadening of the T waves
Prominent U waves
Depressed ST segments
T wave inversion
Atrioventricular block (1st, 2nd, 3rd degree AV blocks)
Cardiac arrest

Note: Hypokalemia also increases the likelihood of digitalis toxicity

Hypokalemia: Treatment
Safest way is with oral potassium.
Intravenous replacement is indicated for patients with severe hypokalemia.
If serum potassium is > 2.5 meq/L, and there are ECG abnormalities, potassium can be given
at a rate of 10 meq/L/hr in concentration that should never exceed 80 meq/L.
For severe deficiency, potassium may be given through a intravenous cutdown.
Occasionally, hypokalemia may be refractory to potassium replacement. Magnesium deficiency
may make potassium correction more difficult. Concomitant magnesium repletion avoids this
problem.

Hypokalemia: Treatment
SEVERITY RECOGNITION MANAGEMENT
Mild Low serum potassium levels Dietary potassium
Rarely symptomatic replacement
+/- EKG manifestations
No arrhythmia
orhemodynamic instability

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Moderate Low serum potassium, usually Intravenous potassium
symptomatic with EKG replacement, maximum
abnormalities dilution of 40 meq/L,
+/- arrhythmia, but running at max rate of 5
hemodynamically stable meq/hr
Severe With arrhythmia and evidence IV potassium
of hemodynamic instability replacement, maximum
dilution of 100 meq/L,
max rate of 10 meq/hr
ORAL POTASSIUM REPLACEMENTS
AMOUNT meq OF K ANION NAMES
LIQUIDS 15 ml 10 Cl 5% Potassium chloride
15 ml 20 Cl 10% Potassium chloride
15 ml 40 Cl 20% Potassium chloride
15 ml 20 Gluconat Potassium gluconate
e
POWDERS Packet 15 Cl K-lor
Packet 20 Cl Potassium chloride
Packet 25 Cl K-lyte
TABLETS 1 8 Cl Slow-K
1 8 Cl Micro-K extencaps
1 10 Cl K-dur 10
1 20 Cl K-dur 20
POTASSIUM CONTENT OF FOODS
VERY HIGH HIGH
(12-20 meq) (5-12 meq)
BEANS Garbanzo beans Kidney beans Navy
Soy beans beans
Lima beans Pinto
beans
FRUIT (1/2 cup or as Papaya (one medium) Apricots (3 halves)
stated) Banana (6”)
Cantaloupe (1/4”)
Honeydew melon (1/4”)
Orange (3”) and orange
juice
Pear (one large)
Prunes (4) and prune
juice
Rhubarb

POTASSIUM CONTENT OF FOODS

VERY HIGH HIGH
(12-20 meq) (5-12 meq)

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VEGETABLES (1/2 cup or Artichoke (one)
as stated) Avocado (1/4)
Brussel sprouts
Carrot (7 ½”) and chard
Ketchup (1 tbsp)
Potato (one baked, one
broiled, 10 fries, ½ cup
mashed)
Pumpkin and spinach
Tomato (one) and tomato
juice

Hyperkalemia
Many are spurious or associated with acidosis
Common practice of repeatedly clenching and unclenching the fist during venipuncture may
raise the potassium concentration by 1-2 meq/L by causing local release of potassium from
forearm muscles.

CAUSES OF HYPERKALEMIA
SPURIOUS Leakage from erythrocytes if separation of serum
from clot is delayed.
Thrombocytosis
Marked leukocytosis
Repeated fist clenching during phlebotomy
Specimen drawn from arm with infusion
DECREASED EXCRETION Renal failure, acute and chronic
Severe oliguria
Renal secretory defects
Adrenocortical insufficiency
Hyporeninemic hypoaldosteronism
Spironolactone, triamterene, ACE-I, trimethoprim,
NSAIDs
CAUSES OF HYPERKALEMIA
SHIFT FROM TISSUES Burns, rhabdomyolysis, hemolysis
Metabolic acidosis
Hyperosmolality
Insulin deficiency
Hyperkalemic periodic paralysis
Succinylcholine, arginine, digitalis toxicity, beta-
adrenergic blockers
EXCESSIVE INTAKE Over treatment, orally or parenterally

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Hyperkalemia: Clinical Findings
Weakness and flaccid paralysis
Abdominal distention and diarrhea
ECG is not a sensitive method, but if abnormalities are present, the most common findings are:
Peaked T waves
ST segment elevation
Tachyarrhythmia / supraventricular tachycardia
Ventricular tachycardia
Ventricular fibrillation
Cardiac arrest

Hyperkalemia: Treatment
Confirm that the elevated level of serum potassium is genuine.
Measure plasma potassium.
Withholding of potassium.
Giving cation exchange resins by mouth or enema: polystyrene sulfate, 40-80 g/day in divided
doses.
Emergent treatment is indicated if cardiac toxicity or muscular paralysis is present, or if
hyperkalemia is severe (> 6.5-7 meq/L) even in the absence of ECG changes.
Insulin plus 10-50% glucose may be employed to deposit potassium with glycogen in the liver.
Calcium may be given intravenously as an antagonist ion.
Stimulate transcellular shifts by giving beta-adrenergic agonist drugs.
Sodium bicarbonate as an emergency measure.
Hemodialysis or peritoneal dialysis.

EMERGENCY TREATMENT OF HYPERKALEMIA

MODALITY MECHANISM ONSET DURATION PRESCRIPTION K
OF ACTION REMOVED
FROM
BODY
Calcium Antagonizes 0-5 1 hour Ca gluconate None
cardiac min 10%, 5-30 ml IV;
conduction CaCl 5%, 5-30
abnormalitie ml IV
s
Bicarbonat Shifts K into 15-30 1-2 hours NaHCO3 44-88 None
e cells min meq IV
Insulin Shifts K into 15-60 4-6 hours SAI, 5-10 u IV, None
cells min plus glucose
50%, 25 g IV
Albuterol Shifts K into 15-30 2-4 hours
Nebulized None
cells min albuterol, 10-20
mg in 4 ml
saline
NON-EMERGENCY TREATMENT OF HYPERKALEMIA
MODALITY MECHANISM OF DURATION PRESCRIPTION K
ACTION OF REMOVED
TREATMENT FROM
BODY

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Loop Increased renal K 0.5-2 hours Furosemide 40-160 mg Variable
diuretic excretion IV or orally with or
without NaHCO3, 0.5-3
meq/kg daily
Sodium Ion exchange 1-3 hours Oral: 15-30 g in 20% 0.5-1 meq/g
polystyrene resin binds K sorbitol (50-100 ml)
sulfonate Rectal: 50 g in 20%
(Kayexalate sorbitol
Hemodialysi Extracorporeal K 48 hours Blood flow > 200-300 200-300
s removal ml/min; Dialysate K = 0 meq
Peritoneal Peritoneal K 48 hours Fast exchange, 3-4 L/hr 200-300
dialysis removal meq
POTASSIUM TRANSCELLULAR SHIFTING CARDIAC STABILIZER
EXCRETION
 Dialysis  Glucose and insulin  Calcium
 Diuretics infusion every 6 gluconate 10%
 Ion- hours via slow IV
exchange  Sodium bicarbonate push every 15
resins infusion every 6 minutes for a
administere hours maximum of
d orally or  Beta-adrenergic three doses
transrectall agonist nebulization
y every 6 hours

Fluid and Electrolyte Management

Calcium
Constitute 2% of body weight, but only 1% of the total body calcium is in solution in body fluid.
In plasma, calcium is present as a non-diffusible complex with protein (33%); as a diffusible but
undissociated complex with anions like citrate, bicarbonate, and phosphate (12%); and as ionized
calcium (55%).
Normal total plasma (or serum) calcium concentration is 8.5 to 10.5 mg/dL.
It is the ionized calcium that is necessary for muscle contraction and nerve function (normal: 4.7
to 5.3 mg/dL).
Hypocalcemia
Seen commonly in critically ill patients due to acquired defects in parathyroid-vitamin D axis.
Results occasionally in hypotension which responds to calcium replacement therapy.

CAUSES OF HYPOCALCEMIA
DECREASED INTAKE OR Malabsorption
ABSORPTION
Small bowel bypass, short bowel
Vitamin D deficit
INCREASED IONS Alcoholism
Chronic renal insufficiency
Diuretic therapy (furosemide or
bumetanide)
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ENDOCRINE DISEASES True and pseudohypoparathyroidism
Calcitonin hypersecretion
PHYSIOLOGIC CAUSES Alkalosis and decreased response to vit. D
Decreased serum albumin
Hyperphosphatemia
Aminoglycosides, loop diuretics, foscarnet

Hypocalcemia: Clinical Findings

Symptoms and Signs:
Extensive spasm of skeletal muscle causing cramps and tetany
Laryngospasm with stridor
Convulsions with paresthesias of the lips and extremities
Abdominal pain
Chvostek’s sign
Trousseau’s sign
Laboratory Findings:
Low serum calcium
Elevated serum phosphorus
Low serum magnesium
Prolonged QT interval on the ECG

Hypocalcemia: Treatment
Severe symptomatic hypocalcemia:
In the presence of tetany, arrhythmias or seizures, calcium gluconate 10% is administered
intravenously for 10-15 minutes or via calcium infusion.
10-15 mg of calcium per kilogram body weight, or 6-8 10-ml vials of 10% calcium gluconate
(558-744 mg of calcium) is added to 1 liter of D5W and infused over 4 to 6 hours.
Asymptomatic hypocalcemia:
Oral calcium and vitamin D preparations
Calcium carbonate is well tolerated and inexpensive.

TREATMENT OF HYPOCALCEMIA
MODALITY AMOUNT OF CALCIUM ONSET DOSE
Intravenous 93 mg (4.7 meq) per 10 Immediat 93-186 mg over 10-15
calcium ml e mins; then 10-15 mg/kg
(Calcium over 4-6 hours.
gluconate)
Oral calcium 40% elemental calcium; < 1 hour 250-500 mg calcium 3 to 5
(calcium 250 mg/624 mg tablet times a day.
carbonate) or
500 mg/1250 mg tablet
or
500 mg/1500 mg tablet

CAUSES OF HYPERCALCEMIA
INCREASED INTAKE OR Milk-alkali syndrome
ABSORPTION Vitamin D or vitamin A excess

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ENDOCRINE DISORDERS
NEOPLASTIC DISEASES
MISCELLANEOUS
CAUSES
Primary and secondary hyperparathyroidism
Acromegaly
Adrenal insufficiency
Tumors producing PTH-related proteins
Metastases to bone
Lymphoproliferative disease
Secretion of prostaglandins and osteolytic
factors
Thiazide diuretics and renal transplant
complications
Sarcoidosis and Paget’s disease of the bone
Hypophosphatasia, immobilization, iatrogenic

Hypercalcemia: Clinical Findings

Symptoms and Signs:
Polyuria and constipation
Stupor, coma and azotemia
Ventricular extrasystoles and idioventricular rhythm
Laboratory Findings:
Significant elevation of serum calcium
Serum phosphorus may or may not be elevated
Shortened QT interval on the ECG
Hypercalcemia: Treatment
Renal excretion of calcium is promoted by giving saline with furosemide.
Treatment of underlying condition.
Fluid and Electrolyte Management

Magnesium
About 50% of total body magnesium exists in the insoluble state in bone.
Only 5% is present as extracellular cation; the remaining 45% is contained in cells as
intracellular cation.
Normal plasma concentration is 1.5-2.5 meq/L, with about one-third bound to protein and two-
thirds existing as free cation.
Excretion is via the kidney

Hypomagnesemia
Nearly half of hospitalized patients have unrecognized hypomagnesemia.
In critically ill patients, arrhythmias and sudden death may be complications.
CAUSES OF HYPOMAGNESEMIA
DIMINISHED ABSORPTION Malabsorption, chronic diarrhea, laxative
OR INTAKE abuse
Prolonged gastrointestinal suction
Small bowel bypass, malnutrition
Alcoholism, parenteral alimentation
INCREASED LOSS DKA, diuretic therapy, diarrhea
Hyperaldosteronism, Bartter’s syndrome
Hypercalciuria

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Renal magnesium wasting
UNEXPLAINED Hyperparathyroidism
Postparathyroidectomy
Vitamin D therapy
Aminoglycoside antibiotics, cisplatin,
amphotericin B

Clinical Findings
Symptoms and Signs:
Weakness
Muscle cramps
CNS hyperexcitability with tremors
Athetoid movements
Jerking, nystagmus
Positive Babinski response
Hypertension, tachycardia and ventricular arrhythmias
Confusion and disorientation

Laboratory Findings:
Decreased serum magnesium levels
Hypocalcemia and hypokalemia
Prolonged QT interval on the ECG
Lengthening of the ST segment on the ECG

Hypomagnesemia: Treatment
Use of IVF containing magnesium as chloride or sulfate, 240-1200 mg/day (10-50 mmol/day)
during the period of severe deficit, followed by 120 mg/day (5 mmol/day) for maintenance.
MgSO4 may also be given intramuscularly in a dosage of 200-800 mg/day (8-33 mmol/day) in
four divided doses.
Serum levels must be monitored.

Hypermagnesemia
Almost always the result of renal insufficiency and the inability to excrete what has been taken
in from food or drugs, especially antacids and laxatives.
Potentially life-threatening as it impairs both central nervous system and muscular function.
Clinical Findings
Symptoms and Signs:
Muscle weakness
Mental obtundation and confusion
Hypotension
Respiratory muscle paralysis or cardiac arrest

Laboratory Findings:
Elevated serum magnesium, BUN, creatinine, K
Decreased serum calcium
Increased PR interval on the ECG
Broadened QRS complex with elevated T waves

Hypermagnesemia: Treatment
Alleviating renal insufficiency
Administration of calcium
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Hemodialysis or peritoneal dialysis

In all things, you shall find everywhere the Acid and the Alcaly.

OTTO TACHENIUS (1620)

Fluid and Electrolyte Management

Acid-Base Disturbances
Arterial Blood Gases
Regulation of pH is accomplished by:
Kidneys
Lungs
Buffer systems
Information obtained from the arterial blood gas measurements:
pH
Partial pressure of carbon dioxide (pCO2)
Partial pressure of oxygen (pO2)
HCO3 level
Oxygen saturation (O2Sat)

Arterial Blood Gases

Normal values:
pH = 7.35 – 7.45
pCO2 = 35 – 45 mmHg
pO2 = 80 – 100 mmHg
HCO3 = 22 – 26 meqs/L
O2Sat > 95%

Steps in obtaining an ABG specimen:

Check the bleeding parameters of the patient.
Prepare the following:
Glass syringe
Heparin (1,000 units/mL)
Alcohol
Cotton balls (soaked with alcohol AND dry)
Container with ice water
Aspirate 1 mL of heparin using a glass syringe
Coat the inner surface of the syringe with heparin, taking care to pull and push the plunger to
make sure heparin evenly coats the syringe.
Expel the excess heparin from the syringe.
Palpate for the radial pulse.
With the needle directed at a slight angle from the vertical, and pointed cephalad, gradually
puncture the site and wait for arterial blood to rush in.
After obtaining the specimen, secure the needle and place the syringe with the specimen in ice
water.
Apply direct pressure on the puncture site for at least one minute, or until bleeding stops using a
dry sterile cotton ball.
Send the specimen directly to the laboratory.
A sample is allowed to stand for a maximum of two hours only.

ABG Interpretation

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SUMMARY OF EXPECTED COMPENSATION FOR SIMPLE ACID-BASE

DISORDERS
DISORDER INITIAL CHANGE COMPENSATORY RESPONSE
Metabolic Decrease in Decrease in pCO2:
Acidosis HCO3- Δ pCO2 = 1.1 – 1.3 (ΔHCO3-)

Metabolic Increase in Increase in pCO2:

Alkalosis HCO3- Δ pCO2 = 0.6 – 0.7 (ΔHCO3-)

Respiratory Increase in pCO2 Increase in HCO3-

Acidosis ACUTE: ΔHCO3-= 0.1 Δ pCO2 + 2
CHRONIC: ΔHCO3-= 0.3 – 0.35 Δ pCO2
Respiratory Decrease in Decrease in HCO3-
Alkalosis pCO2 ACUTE: ΔHCO3-= 0.2 – 0.25 Δ pCO2
CHRONIC: ΔHCO3-= 0.4 – 0.5 Δ pCO2

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