Fluid & Electrylyte tables

8/7/2019 Fluid & Electrylyte tables

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Table 46-2 Major Electrolytes

Electrolyte Functions Sources and Losses Regulation

Sodium (Na+): chief

electrolyte of ECF that

moves easily betweenintravascular and

interstitial spaces and

moves across cell

membranes by activetransport; influential in

many chemical reactions

in the body, particularly

in nervous tissue cells

and muscle tissue cells

Controls and regulates the

volume of body fluids

Maintains water balancethroughout the body

Is the primary regulator of

ECF volume

Influences ICF volumeParticipates in the

generation and transmission

of nerve impulses

Is an essential electrolyte in

the sodium-potassium pump

The average daily requirements

for sodium not known

Precisely; 2,400 mg (approx. 1tsp) as the Daily Value cited on

the Nutrition Facts label; RDA

for sodium for adults about 500

mg, or 0.5 gSodium found in many foods;

typically present in large

amounts, particularly in bacon,

ham, sausage, catsup, mustard,

relish, processed cheese, canned

vegetables, bread, cereal, and

salted snack foods; also in table

salt (sodium chloride; about46% sodium)

Sodium excesses eliminated

primarily by the kidneys; small

amounts lost in feces and

perspiration

Sodium normally maintained

in the body within a

relatively narrow range;deviations quickly resulting

in a serious health problem

Sodium concentrations

affected by salt, as well aswater, intake

Sodium conserved through

reabsorption in the kidneys, a

process stimulated by

aldosterone

The normal extracellular

concentration of sodium:

135–145 mEq/L (mmol/L).

Potassium (K +): major

cation of ICF working in

reciprocal fashion with

sodium (eg, an excessive

intake of sodium

resulting in an excretion

of potassium, and vice

versa)

Is the chief regulator of

cellular enzyme activity and

cellular water content

Plays a vital role in such

processes as the

transmission of electric

impulses, particularly in

nerve, heart, skeletal,intestinal, and lung tissue;protein and carbohydrate

metabolism; and cellular

building

Assists in regulation of

acid-base balance by

cellular exchange with H+


not known precisely; an intake

of 50 to 100 mEq daily enough

to maintain K + balance

Adequate quantities usually in a

wellbalanced diet

Leading food sources: bananas,

peaches, kiwi, figs, dates,apricots, oranges, prunes,melons, raisins, broccoli, and

potatoes. Meat and dairy

products also with adequate

amounts of potassium

Potassium excreted primarily by

the kidneys (no effective

method of conserving

potassium); deficits occur if potassium excretion in excess

without being replaced

simultaneously.

Gastrointestinal (GI) secretionscontain potassium in large

quantities; also some in

perspiration and saliva

Conservation of cellular K +

by the sodium pump

(described later in the

chapter) when Na+ is

excluded; conservation by

kidneys when cellular K +

decreased.

Aldosterone secretiontriggering K + excretion inurine

Normal range for serum

potassium: 3.5 to 5 mEq/L

Calcium (Ca2+): most Is necessary for nerve Average daily requirement Increased secretion of



abundant electrolyte in

the body, with up to 99%

of the total amount of calcium in the body

found in bones and teethin ionized form; close

link between

concentrations of calcium

and phosphorus

impulse transmission and

blood clotting

Is a catalyst for musclecontraction

Is needed for vitamin B12absorption and for its use

by body cells

Acts as a catalyst for many

cell chemical activities

Is necessary for strong

bones and teethDetermines the thickness

and strength of cellmembranes

about 1 g for adults; higher

amounts according to body

weight required for children andpregnant and lactating women

Consumption of 1,500 mg/dayrecommended for older adults,

particularly postmenopausal

women and men older than 65

years of age

Sources include milk, cheese,

and dried beans; some presentin meats and vegetables

The use of calcium stimulatedby vitamin D; most active form

of vitamin D (calcitriol)

responsible for promoting

calcium absorption and limiting

calcium excretion when levels

are inadequate

Movement out of bones and

teeth to maintain normal bloodcalcium levels, if necessary.

Excretion via urine, feces, bile,

digestive secretions, and

perspiration

parathyroid hormone (PTH),

to increase the release of

calcium from bones into theblood and to increase

reabsorption from kidneysand intestine when ECF

levels are decreased

A high serum phosphate

concentration, resulting in

decreased serum calcium

level; a low serum phosphateconcentration leading to

increased serum calciumCalcitonin, a hormone

secreted by the thyroid gland,

exerting an effect on calcium

opposite that of PTH.

Increases in calcitonin

resulting in reduced serum

calcium concentration

primarily by opposingosteoclast bone resorption

Magnesium (Mg2+): most

of cation magnesium

found within body cells

—heart, bone, nerve, and

muscle tissues; secondmost important cation in

the ICF

Is important for the

metabolism of

carbohydrates and proteins

Is important for many vital

reactions involvingenzymes

Is necessary for protein and

DNA synthesis, DNA andRNA transcription, and

translation of RNA

Maintains normal

intracellular levels of

potassium

Helps maintain electrical

activity in nervous tissue

membranes and muscle

membranes

The average daily adult

requirement about 18–30 mEq,

with children requiring larger

amounts

Magnesium found in mostfoods, but especially in

vegetables, nuts, fish, whole

grains, peas, and beans

Intestinal absorption and

excretion by kidneys

Plasma concentrations of

magnesium ranging from

1.3–2.1 mEq/L, with aboutone third of that amount

bound to plasma proteins

Chloride (Cl-): chief

extracellular anion, found

in blood, interstitial fluid,

and lymph and in minute

amounts in ICF

Acts with sodium to

maintain the osmotic

pressure of the blood

Plays a role in the body's

acid-base balanceHas important buffering


of chloride unknown

Found in foods high in sodium,

dairy products, and meat

Normally paired with

sodium; exerted and

conserved with sodium by the

kidneys

Chloride deficits lead topotassium deficits, and vice



action when oxygen and

carbon dioxide exchange in

red blood cellsIs essential for the

production of hydrochloricacid in gastric juices

versa

Normal serum chloride

levels: from 95–105 mEq/L(mmol/L)

Bicarbonate (HCO3-): an

anion that is the major

chemical base buffer

within the body; found in

both ECF and ICF

Is essential for acid-basebalance; bicarbonate and

carbonic acid constitute the

body's primary buffer

system

Losses possible via diarrhea,diuretics, and early renal

insufficiency; excess possible

via overingestion of acid

neutralizers, such as sodium

bicarbonate

Bicarbonate levels regulatedprimarily by the kidneys

Bicarbonate readily available

as a result of carbon dioxide

formation during metabolism

Normal bicarbonate levels

range between 25 and 29

mEq/L (mmol/L)

Phosphate (PO4-): the

major anion in body

cells; a buffer anion in

both ICF and ECF

Helps maintain the body's

acid-base balance

Is involved in important

chemical reactions in the

body; eg, phosphorus is

necessary for many B

vitamins to be effective,helps promote nerve and

muscle action, and plays a

role in carbohydrate

metabolism

Is important for cell

division and for the

transmission of hereditarytraits

Average daily requirements for

phosphorus similar to those for

calcium

Found in most foods but

especially in beef, pork, and

dried peas and beans

Metabolism the same ascalcium

Regulation by PTH and by

activated vitamin D

Calcium and phosphate

inversely proportional; an

increase in one results in a

decrease in the other

Normal range of phosphate:2.5 to 4.5 mEq/L (mmol/L)



Table 46-3 Homeostatic Mechanisms That Maintain the Composition and Volume of Body Fluid

Within Narrow Limits of Normal

Organs of

Homeostasis Functions

Kidneys • Regulate extracellular fluid (ECF) volume and osmolality by selective retention and

excretion of body fluids

• Regulate electrolyte levels in the ECF by selective retention of needed substances and

excretion of unneeded substances

• Regulate pH of ECF by excretion or retention of hydrogen ions

• Excrete metabolic wastes (primarily acids) and toxic substances

Heart and

blood vessels

• Circulate blood through the kidneys under sufficient pressure for urine to form (pumping

action of the heart)

• React to hypovolemia by stimulating fluid retention (stretch receptors in the atria and

blood vessels)

Lungs • Eliminate about 13,000 mEq of hydrogen ions (H+) daily, as opposed to only 40 to 80

mEq excreted daily by the kidneys

• Act promptly to correct metabolic acid–base disturbances; regulate H+ concentration (pH)

by controlling the level of carbon dioxide (CO2) in the extracellular fluid as follows:

1. Metabolic alkalosis causes compensatory hypoventilation, resulting in CO2

retention (increases acidity of the extracellular fluid).

2. Metabolic acidosis causes compensatory hyperventilation, resulting in CO2

excretion (decreases acidity of the extracellular fluid).

• Remove approximately 300 mL of water daily through exhalation (insensible water loss)

in the normal adult



Adrenal

glands• Regulate blood volume and sodium and potassium balance by secreting aldosterone, a

mineral corticoid secreted by the adrenal cortex

1. The primary regulator of aldosterone appears to be angiotensin II, which is

produced by the renin–angiotensin system. A decrease in blood volume triggers

this system and increases aldosterone secretion, which causes sodium retention(and thus water retention) and potassium loss.

2. Decreased secretion of aldosterone causes sodium and water loss and potassium

retention.

• Cortisol, another adrenocortical hormone, has only a fraction of the potency of

aldosterone.

• However, secretion of cortisol in large quantities can produce sodium and water retention

and potassium deficit.

Pituitary

gland• Stores and releases the antidiuretic hormone (ADH), which makes the body retain water;

functions of ADH include:

1. Maintains osmotic pressure of the cells by controlling renal water retention or excretion

a. When osmotic pressure of the ECF is greater than that of the cells (as in

hypernatremia—excess sodium—or hyperglycemia), ADH secretion is

increased, causing renal retention of water.

b. When osmotic pressure of the ECF is less than that of the cells (as in

hyponatremia), ADH secretion is decreased, causing renal excretion of

water.

2. Controls blood volume (less influential than aldosterone)a. When blood volume is decreased, an increased secretion of ADH results

in water conservation.

b. When blood volume is increased, a decreased secretion of ADH results

in water loss.

Nervous

system• Inhibits and stimulates mechanisms influencing fluid balance; acts chiefly to regulate

sodium and water intake and excretion

• Regulates oral intake by sensing intracellular dehydration, which triggers thirst (thirst

center located in hypothalamus)

Parathyroid

glands• Regulate calcium (Ca2+) and phosphate (HPO4

2-) balance by means of parathyroid

hormone (PTH); PTH influences bone reabsorption, calcium absorption from the

intestines, and calcium reabsorption from the renal tubules.

1. Increased secretion of PTH causes:a. Elevated serum calcium concentration

b. Lowered serum phosphate concentration

2. Conversely, decreased secretion of PTH causes:a. Lowered serum calcium concentration

b. Elevated serum phosphate concentration



Table 46-4 Acid–Base Parameters for Arterial Blood Gas Studies

Normal Acid Base

pH 7.35–7.45 <7.35 >7.45

PaCO2 35–45 mm Hg >45 mm Hg <35 mm Hg

HCO3- 22–26 mEq/L <22 mEq/L >26 mEq/L



Focused Assessment Guide 46-1 Fluid, Electrolyte, and Acid–Base Balance

Factors to Assess Questions and Approaches

Usual patterns of fluid intake Describe the amount and types of fluids you usually drink in a 24-hour period. Have there been any recent changes?

Usual pattern of fluid elimination Describe your usual voiding/urination habits.

Any recent changes in frequency or amount?

Is your body losing fluids in any other major way?

• Vomiting

• Diarrhea

• Excessive perspiration

• Fistula

Patient's evaluation of hydration

status

Do you think there is an approximate balance between your fluid

intake and output?

Have you noticed any signs that your body is experiencing too

much or too little hydration (difficulty breathing, edema, dry skin

and mucous membranes, thirst)?

History of disease process Is there any history of disease process or injury that might disrupt

fluid and electrolyte balance (eg, diabetes mellitus, cancer, burns)?

Medication/nutrition history Do you take any medications or treatments that might disrupt fluid

and electrolyte balance (eg, steroids, diuretics, total parenteral

nutrition, dialysis)?

Have you been trying to lose weight by dieting, using diuretics,

laxatives, or diet aids?

Have you been following a high-protein, low-carbohydrate diet?



Fluid, electrolyte, and acid–base

imbalances and contributing

factors

Are you aware of any other fluid balance problems you may be

experiencing?

• Nature

• Onset of problem and frequency• Causes

• Severity

• Symptoms

• Intervention attempted and results

Table 46-5 Imbalances Resulting From Loss of Specific Body Fluid

Fluid Lost Imbalances Likely to Occur Fluid Lost Imbalances Likely to Occur

Gastric juice Extracellular fluid volume deficit

Metabolic alkalosis

Sodium deficitPotassium deficit

Pancreatic juice Metabolic acidosis

Sodium deficit

Calcium deficitExtracellular fluid volume deficit

Tetany (if metabolic alkalosis is present) Sensible perspiration Extracellular fluid volume deficit

Sodium deficit

Ketosis of starvation

Magnesium deficit

Insensible water loss Water deficit (dehydration)

Sodium excess

Intestinaljuice

Extracellular fluid volume deficit

Metabolic acidosis

Sodium deficit

Potassium deficit

Wound exudate Protein deficit

Sodium deficit


Bile Sodium deficit

Metabolic acidosis

Ascites Protein deficit

Sodium deficitPlasma-to-interstitial fluid shift




Table 46-6 Parameters to Be Considered in Clinical Assessment for Fluid, Electrolyte, and Acid–Base Balance

Assessment

Parameters Nursing Considerations Findings in Healthy Adult Significant Findings

Comparison of

total intake and

output of fluids

Records may be initiated by the nurse

for any patient with a real or potential

water or electrolyte problem.

Intake should include all fluids

taken into the body.

Output should include urine,

vomitus, diarrhea, drainage from

fistulas, and drainage from suction

apparatus. Perspiration and drainage

from lesions should be noted andestimated. Prolonged

hyperventilation should also be

noted because it is an important

route of water vapor loss.

Fluid intake about equals fluid

output—when averaged over 2 or 3

days.

Range of 1500–3500 mL fluid

intake and loss; 2000 mL is average

adult intake and loss per day.

Output of urine normally

approximates the ingestion of

liquids; water from food and

oxidation is balanced by the water loss through feces, the skin, and the

respiratory process.

When the total intake is substantiall

less than the total output, the patient

in danger of fluid volume deficit.

When the total intake is substantiall

more than the total output, the patien

in danger of fluid volume excess.

Urine volume and

concentration

All fluid losses are measured

according to routes.

A device calibrated for small

volumes of urine is used when

hourly urine volumes need to be

measured.

Factors that can alter urinary output

must be accounted for:

Amount of fluid intake

Losses from skin, lungs, and GI tract

Amount of waste products for

excretions

Normal urinary output is about 1

mL/kg of body weight per hour (for

the average adult: 1500 mL/24 hr,

which is equivalent to about 40–80

mL/hr).

Stress may diminish the 24-hour urine volume in the adult to 750–

1000 mL (or 30–50 mL/hr) because

of increased aldosterone and ADH

secretion.

The range of specific gravity is from

1.003 to 1.035. Urine osmolality

ranges between 500 mOsm and 800

mOsm/ kg (mmol/kg).

A low urine volume with a high

specific gravity indicates fluid volum

deficit.

A low urine volume with a low spec

gravity indicates renal disease.

A high urine volume suggests fluidvolume excess.

Urine volume is increased in condit

with high solute loads, such as diabemellitus.

Hypovolemia causes decreased rena

perfusion and thus oliguria;hypervolemia causes increased urina

volume if the kidneys are functionin



Renal concentrating ability

Blood volume

Hormonal influences (primarily

aldosterone and ADH)

normally.

Body weight Because of the common

inaccuracies in recording intake and

output, body weight is believed to

be a more accurate indicator of fluid

gained and lost.

Guidelines for weighing patients

include:

Using the same scale each time.

Measuring weight at the same time

each day: in the morning before

breakfast and after voiding.

Ensuring the patient is wearing the

same or similar clothing (clothing

should be dry).

Using a bed scale if the patient is

unable to stand on a small, portablescale.

A patient may have a severe fluid

volume deficit even though body

weight is essentially unchanged

when there is a third-space loss of

body fluid.

A patient's dry weight should

remain relatively stable.

Rapid variations in weight closely

reflect changes in body fluid volum

A rapid loss of body weight occurs

when the total fluid intake is less tha

the total fluid output.

Rapid loss of 2% total body weight

(TBW) indicates mild fluid volume

deficit.

Rapid loss of 5% TBW indicates

moderate fluid volume deficit.

Rapid loss of 8% or more of TBWindicates severe fluid volume deficit

A rapid gain of body weight occurs

when the total fluid intake is greater

than the total fluid output.

Rapid gain of 2% TBW indicates m

fluid volume excess.

Rapid gain of 5% TBW indicates

moderate fluid volume excess.

Rapid gain of 8% or more of TBW

indicates severe fluid volume excess

A rapid gain or loss of 1 kg (2.2 lb)

body weight is about equal to the ga

or loss of 1 L of fluid.



Skin turgor

(elasticity)

The patient's skin over the sternum,

inner aspect of the thighs, or

forehead is pinched.

Some prefer to test skin turgor inchildren over the abdominal area

and on the medial aspect of the

thighs.

Skin turgor can vary with age,

nutritional state, and even race andcomplexion.

Pinched skin immediately falls back

to its normal position when

released.

Reduced skin turgor is common inolder patients (those more than 55–

60 years of age) because of a

primary decrease in skin elasticity.

In a person with a fluid volume defi

the skin flattens more slowly after th

pinch is released; the skin may remaelevated for many seconds.

Severe malnutrition, particularly in

infants, can cause depressed skin tur

even in the absence of fluid depletio

Tongue turgor Unlike skin turgor, tongue turgor is

not affected appreciably by age and

thus is a useful assessment for all

age groups. (In an arid climate, thismay not be a reliable parameter.)

Tongue has one longitudinal furrow.In the person with fluid volume defi

there are additional longitudinal

furrows and the tongue is smaller.

Sodium excess causes the tongue to

look red and swollen.

Moisture and oral

cavity

A dry mouth may be the result of

fluid volume deficit or of mouthbreathing. (Exposure to an arid

climate may result in a dry mouth.)

Mucous membranes in oral cavity

are moist.

Dryness of the membrane where the

cheek and gum meet indicates fluidvolume deficit.

Dry sticky mucous membranes are

noted in sodium excess. (The oral

cavity feels like flypaper.)

Tearing and

salivation

Tearing and salivation decrease

normally with age.

The absence of tearing and salivatio

a child is a sign of fluid volume defi

it becomes obvious with a fluid loss

5% of TBW.

Appearance of

skin and skin

temperature

Metabolic acidosis can cause warm,

flushed skin (due to peripheral

vasodilation).

Facial appearance A person with a severe fluid volume

deficit may have a pinched and drawfacial expression.



A fluid volume deficit of 10% of boweight causes decreased intraocular

pressure, causing the eyes to appear

sunken and to feel soft to the touch.

Edema (excessive

accumulation of

interstitial fluid)

Pitting edema (see Fig. 46-7)

Measurement of an extremity or

body part with a millimeter tape, in

the same area each day, is a more

exact method of measurement.

An excess of interstitial fluid may

accumulate predominantly in thelower extremities of ambulatory

patients and in the presacral regionof bedridden patients.

The presence of periorbital (around

the eyes) edema or pedal edema

should prompt one to look for

edema in other parts of the body.

No edema Clinically edema is not usually

apparent in the adult until the retent

of 5–10 lb of excess fluid occurs.

Pitting edema is not evident until at

least a 10% increase in weight has

occurred.

Formation of edema may be localize(as in thrombophlebitis) or generaliz

(as in heart failure, cirrhosis of livernephrotic syndrome). Edema of

congestive heart failure, liver cirrho

or nephrotic syndrome is the result o

sodium retention.

Body temperature Because fever increases the loss of

body fluids, it is important that

temperature elevations be detected

early and appropriate interventions

be taken.

Body temperature and other vital

signs should be assessed as ordered

and at the nurse's discretion.

Baseline temperature: diurnal

variations

There is an elevation of body

temperature in hypernatremia

(dehydration) probably related to la

of available fluid for sweating.

There is a decrease in body temperain fluid volume deficit, when

uncomplicated by infection.

Fever increases the loss of body flui

A temperature elevation between 10(38.3°C) and 103°F (39.4°C) increa

the 24-hour fluid requirement by at

least 500 mL, and a temperature abo

103°F increases it by at least 1000 m

Pulse Baseline pulse rate, rhythm, and

volume

Tachycardia is usually the earliest si

of the decreased vascular volumeassociated with fluid volume deficit

Irregular pulse rates also occur with

potassium imbalances and magnesiu

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Measures the levels to which theveins are distended on the neck or

above the level of the manubrium

More accurate assessments of blood

volume are obtained by measuring

CVP by hemodynamic monitoring.

Neuromuscular

irritability

When imbalances in calcium,

magnesium, and sodium are

suspected it is important to assess

patients for increased or decreased

neuromuscular irritability.

Negative response

To test for Chvostek's sign, thefacial nerve should be

percussed about 2 cm anterior

to the ear lobe.

Negative response Patients with hypocalcemia or hypomagnesemia respond positively

with a unilateral twitching of the fac

muscles, including the eyelid and lip

To test for Trousseau's sign, a

blood pressure cuff is placed

on the arm and inflated above

systolic pressure for 3 minutes.

The response in the prospective

muscle is a sudden contraction (2+).

A positive response is the developm

of carpal spasm.

A deep tendon reflex is elicited

by briskly tapping a partially

stretched tendon with a rubber

percussion hammer, preferably

over the tendon insertion of the

muscle.

Reflexes usually are graded on a 0

to 4+ scale.

0 = no response

1+ = somewhat diminished, but

present

2+ = normal

3+ = brisker than average and

possibly but not necessarilyindicative

of disease

4+ = hyperactive

Deep tendon reflexes may be

hyperactive in the presence of

hypocalcemia, hypomagnesemia,

hypernatremia, and alkalosis.

The muscle being tested

should be slightly stretched,

and the patient should be

relaxed.

Deep tendon reflexes may be

hypoactive in the presence of

hypercalcemia,

hypermagnesemia, hyponatremia

hypokalemia, and acidosis.

Behavior

Sensation Fatiguelevel

Because these changes are often

vague, they are best evaluated incontext with specific imbalances

.



Table 46-7 Acid–Base Disturbances



Risk Factors Assessments Nursing Interventions

Respiratory Acidosis (Carbonic Acid Excess)

Acute respiratory disease:Pulmonary edema

Aspiration of a foreign

body

AtelectasisOverdose of sedative or

anesthetic

Cardiac arrest

Chronic respiratory disease:

Emphysema

Bronchial asthma

Cystic fibrosis

Inadequate mechanical

ventilation

CNS depressionNeuromuscular disease

Acute respiratory acidosisMental cloudiness

Dizziness

Muscular twitching

UnconsciousnessABGs

pH <7.35

PaCO2 >45 mm Hg

(primary)

HCO3- normal or only

slightly elevated

Chronic respiratory acidosis

Weakness

Dull headache

ABGspH <7.35 or low N

PaCO2 >45 mm Hg

(primary)

HCO3- >26 mEq/L

(compensatory)

Treatment is directed at improving ventilation:Pharmacologic measures

Pulmonary hygiene measures

Adequate hydration

Supplemental oxygenMechanical ventilation may be necessary to correct disorder but

must be used cautiously to decrease PaCO2 slowly.

Respiratory Alkalosis (Carbonic Acid Deficit)

Hyperventilation

Extreme anxiety (most

common cause)Hypoxemia

High fever

Early sepsis

Excessive ventilation by

mechanical ventilator

CNS lesion involving the

respiratory center Thyrotoxicosis

Lightheadedness

Inability to concentrate

Hyperventilation syndromeTinnitus

Palpitations

Sweating

Dry mouth

Tremulousness

Convulsions and loss of

consciousnessABGs

pH >7.45

PaCO2 <35 mm Hg

(primary)

HCO3- <22 mEq/L

(compensatory)

If anxiety is the cause, the patient should be encouraged to breathe

more slowly (causes accumulation of CO2) or breathe into a closed

system (paper bag). Sedative may also be necessary in extremeanxiety.

Treatment of other causes is directed at correcting the underlying

problem.

Metabolic Acidosis (Base Bicarbonate Deficit)

Diarrhea

Intestinal fistulas

Headache

Confusion

Treatment is directed toward correcting the metabolic deficit. If

the cause of the problem is excessive intake of chloride, treatment



Ureterosigmoidostomy

Hyperalimentation

Excessive intake of acids,such as salicylates

Diabetic ketoacidosisRenal failure

Starvational ketoacidosis

Drowsiness

Increased respiratory rate

and depthNausea and vomiting

Peripheral vasodilationABGs

pH <7.35

HCO3- <22 mEq/L

(primary)

PaCO2 <35 mm Hg

Hyperkalemia frequentlypresent

obviously focuses on eliminating the source. When necessary,

bicarbonate is administered.

Metabolic Alkalosis (Base Bicarbonate Excess)

Vomiting or gastric suction

Hypokalemia

Potassium-wasting diuretics

Alkali ingestion

(bicarbonate-containing

antacids)

Renal loss of H+ (eg, from

steroid or diuretic use)

Dizziness

Tingling of fingers and toes

Hypertonic muscles

Depressed respirations

(compensatory)

ABGs

pH >7.45

HCO3- >26 mEq/L

(primary)

PaCO2 >45 mm Hg

(compensatory)

Hypokalemia may be

present

Treatment is aimed at reversal of the underlying disorder.

Sufficient chloride must be supplied for the kidney to absorb

sodium with chloride (allowing the excretion of excess

bicarbonate). Treatment also includes administration of NaCl

fluids to restore normal fluid volume.

Table 46-8 Fluid Volume Disturbances




Fluid Volume Deficit (Hypovolemia)

GI: Vomiting, diarrhea, suction, fistulasHemorrhage

Excessive sweating

Skin trauma, burns, draining wounds

Third-space fluid shiftsExcessive laxative or diuretic use

Polyuria from renal disease or diuretics

Hyperglycemia

Change in mental status (unable to gain access

to fluids, depression, confusion)

ThirstWeight loss over short period

Weakness, fatigue, anorexia

Dry mucous membranes

Poor skin and tongue turgor Sunken eyes

Flat neck veins

Urine output <30 mL/hr

Postural hypotension

Weak, rapid pulse

↑Urine specific gravity

↑Hematocrit

↑BUN

↑Serum sodium

Altered sensorium

Assess for presence or worsening of FVD.Administer oral fluids if indicated.

If patient unable to eat and drink, anticipate

TPN or tube feedings to be ordered.

Monitor patient's response to fluid intake,either oral or parenteral.

Be alert for signs of fluid overload.

Provide appropriate skin care.

Fluid Volume Excess (Hypervolemia)

Compromised regulatory mechanisms: renal

failure, CHF, cirrhosis of liver, Cushing's

syndrome

GI irrigation with hypotonic fluid

Excess IV fluids with sodium

Corticosteroid therapy

Excessive ingestion of sodium-containing

substances in diet or sodium-containingmedications

Weight gain over short

period

Peripheral edema (may be

pitting)

Increased BP

Shortness of breath

Crackles and wheezes in

lungsFull, bounding pulse

Neck vein distention

Polyuria if renal function is

normal

Ascites, pleural effusion

Pulmonary edema

↓BUN (due to plasmadilution)

↓Hematocrit

↓Serum sodium

↓Urine specific gravity

Assess for presence or worsening of FVE.

Encourage adherence to sodium-restricted

and fluid-restricted diet, if ordered.

Avoid OTC drugs or check with physician or

pharmacist about sodium content.

Encourage rest periods.

Monitor patient's response to diuretics.

Teach self-monitoring of weight and intakeand output.

Attentive skin care.

Monitor respiratory status.

Table 46-9 Electrolyte Disturbances




Hyponatremia

Loss of sodium, as in:Loss of GI fluids

Use of diuretics

Adrenal insufficiency

Gains of water, as in:Excessive administration of

D5W

Water intoxication

Disease states associated with

SIADH (a form of

hyponatremia)

Pharmacologic agents that may

impair water excretion

AnorexiaNausea and vomiting

Lethargy

Confusion

Muscle crampsMuscular twitching

Seizures

Coma

Serum Na below 135 mEq/L

Urine specific gravity <1.010

Monitor fluid losses and gains.Monitor for presence of GI and CNS

symptoms.

Monitor serum Na levels.

Check urine specific gravity.If able to eat, encourage foods and fluids with

high sodium content.

Be aware of sodium content of common IV

fluids.

Avoid giving large water supplements to

patients receiving isotonic tube feedings.

Take seizure precautions when hyponatremia

is severe.

Hypernatremia

Water deprivationIncreased sensible and insensible

water loss

Ingestion of large amount of salt

Excessive parenteral

administration of sodium-

containing solutions

Profuse sweating

Diabetes insipidus

ThirstElevated body temperature

Tongue dry and swollen, sticky mucous

membranes

Severe hypernatremia

Disorientation

Hallucinations

Lethargy when undisturbed

Irritable and hyperactive

Focal or grand mal seizuresComa

Serum Na above 145 mEq/L

Urine specific gravity >1.015

Monitor fluid losses and gains.Observe for excessive intake of high sodium

foods.

Monitor sodium content of prescriptions and

OTC drugs.

Monitor for changes in behavior such as

restlessness, lethargy, and disorientation.

Look for excessive thirst and elevated body

temperature.

Monitor serum Na levels.Check urine specific gravity.

Give sufficient water with tube feedings to

keep serum Na and BUN at normal limits.

Hypokalemia

Diarrhea

Vomiting or gastric suction

Potassium-wasting diureticsSteroid administration and

certain antibioticsPoor intake as in anorexia

nervosa, alcoholism, potassium-

free parenteral fluids

Polyuria

Fatigue

Anorexia, nausea, and vomiting

Muscle weaknessDecreased bowel motility

Cardiac arrhythmiasIncreased sensitivity to digitalis

Polyuria, nocturia, dilute urine

Postural hypotension

Serum K below 3.5 mEq/L

ECG changes

Paresthesias or tender muscles

Monitor for occurrence of hypokalemia.

Assess digitalized patients at risk for

hypokalemia, which potentiates the action of digitalis

Prevent hypokalemia by:Encouraging extra K intake if possible

Educating about abuse of laxatives and

diuretics

Administer oral K supplements if ordered.

Be knowledgeable about danger of IV

potassium administration.



Hyperkalemia

Decreased potassium excretion:

Oliguric renal failurePotassium-sparing diuretics

Hypoaldosteronism

High potassium intake,

especially in presence of renalinsufficiency

Shift of potassium out of cells

(acidosis, tissue trauma,

malignant cell lysis)

Vague muscle weakness

Cardiac arrhythmiasParesthesias of face, tongue, feet, and

hands

Flaccid muscle paralysis

GI symptoms such as nausea, intermittentintestinal colic, or diarrhea may occur

Serum K above 5.0 mEq/L

Monitor for hyperkalemia, which is life-

threatening.Prevent hyperkalemia by:

Following rules for safe administration of K

Avoiding giving patients with renal

insufficiency K-saving diuretics, K supplements, or salt substitutes

Cautioning about foods high in potassium

content

Hypocalcemia

Surgical hypoparathyroidismMalabsorption

Vitamin D deficiency

Acute pancreatitis

Excessive administration of citrated blood

Alkalotic states

Trousseau's and Chvostek's signsNumbness and tingling of fingers and toes

Mental changes

Seizures

Spasm of laryngeal musclesECG changes

Cramps in muscles of extremities

Total serum calcium <8.5 mg/dL

Take seizure precautions when hypocalcemiais severe.

Monitor condition of airway.

Take safety precautions if confusion is

present.Educate people at risk for osteoporosis about

need for dietary calcium intake.

Discuss calcium-losing aspects of nicotine

and alcohol use.

Hypercalcemia

Hyperparathyroidism

Malignant neoplastic disease

Prolonged immobilizationLarge doses of vitamin D

Overuse of calcium supplements

Thiazide diuretics

Muscular weakness

Tiredness, lethargy

ConstipationAnorexia, nausea, and vomiting

Decreased memory and attention span

Polyuria and polydipsia

Renal stones

Neurotic behavior

Cardiac arrest

Serum calcium >10.5 mg/dL

Increase mobilization when feasible.

Encourage sufficient oral intake.

Discourage excessive consumption of milk products.

Encourage bulk in the diet.

Take safety precautions if confusion is

present.

Be alert for signs of digitalis toxicity in

hypercalcemic patients.

Force fluids to prevent formation of renal

stones.

Hypomagnesemia

Chronic alcoholismIntestinal malabsorption

Diarrhea

Nasogastric suction

Neuromuscular irritabilityIncreased reflexes

Coarse tremors

Seizures

Assess for magnesium deficit because itpredisposes patient to digitalis toxicity.

Take seizure precautions if necessary.

Monitor condition of airway because



Drugs

Thiazide diuretics

Aminoglycoside antibioticsExcessive doses of vitamin D

Citrate preservative in blood

Cardiac manifestations

Tachyarrhythmias

Increased susceptibility to digitalistoxicity

Mental changesDisorientation

Mood changes

Serum magnesium <1.3 mEq/L

laryngeal stridor can occur.

Educate patient if abuse of diuretics or

laxatives is a problem.Educate about intake of foods rich in

magnesium.

Hypermagnesemia

Renal failure

Adrenal insufficiencyExcessive magnesium

administration during treatmentof eclampsia

Hemodialysis with hard water or

dialysate high in magnesium

content

Early sign is serum magnesium level of 3

to 5 mEq/LFlushing and sense of skin warmth

HypotensionDepressed respirations

Drowsiness, hypoactive reflexes, and

muscular weakness

Cardiac abnormalities

If hypermagnesemia is present, be alert for

low BP and shallow respirations, lethargy,drowsiness, and coma.

Do not give magnesium-containingmedications to patient with renal failure or

compromised renal function.

Be cautious of OTC drugs.

Check deep tendon reflexes frequently.

Hypophosphatemia

Glucose administration

Refeeding after starvation

HyperalimentationAlcohol withdrawal

Diabetic ketoacidosis

Respiratory alkalosis

Cardiomyopathy

Acute respiratory failure

SeizuresDecreased tissue oxygenation

Joint stiffness

Serum phosphate <2.5 mg/dL

Be aware that severely hypophosphatemic

patients are at greater risk for infection.

Administer IV phosphate products cautiously.Introduce hyperalimentation cautiously in

patients who are malnourished.

Monitor for diarrhea when taking oralsupplements.

Sudden increase in serum phosphate level can

cause hypocalcemia.

Hyperphosphatemia

Renal failureChemotherapy

Large intake of milk

Excessive intake of phosphate-

containing laxatives (Fleetphosphosoda)

Large vitamin D intake

Hyperthyroidism

Short-term consequences:Symptoms of tetany, such as tingling of

the fingertips and around the mouth,

numbness, and muscle spasms

Long-term consequences:Precipitation of calcium phosphate in

nonosseous sites, such as the kidneys,

joints, arteries, skin, or cornea.

Serum phosphate above 4.5 mg/dL

Monitor for signs of tetany.Be aware that soft tissue calcification can be a

long-term complication of chronically

elevated serum phosphate levels.

Instruct patients that use of phosphate-containing laxatives can result in

hyperphosphatemia.

Avoid foods high in phosphorus content.



Table 46-10 Selected IV Solutions



Solution Comments

Isotonic Solutions

5% dextrose in water

(D5W)

Supplies about 170 cal/L and contains 50 g of glucose

Should not be used in excessive volumes because it does not contain any sodium; thus the fluid dilutes the amount of sodium in the serum. Brain swelling, or hyponatremic encephalopathy, can develop rapidly and cause death unless it ispromptly recognized and treated.

0.9% NaCl (normalsaline)

Not desirable as routine maintenance solution because it provides only Na+ and Cl-, which are provided in excessiveamounts.May be used to expand temporarily the extracellular compartment if circulatory insufficiency is a problem; also used to

treat diabetic ketoacidosis.

Lactated Ringer's

solution

A roughly isotonic solution that contains multiple electrolytes in about the same concentrations as found in plasma (no

that this solution is lacking in Mg2+ and PO43-)

Used in the treatment of hypovolemia, burns, and fluid lost as bile or diarrhea

Useful in treating mild metabolic acidosis

Hypotonic Solutions

0.33% NaCl 1/3-strength saline)

A hypotonic solution that provides Na+, Cl-, and free water Na+ and Cl- allows kidneys to select and retain neededamounts

Free water desirable as aid to kidneys in elimination of solutes

0.45% NaCl ½-strength

saline)

A hypotonic solution that provides Na+, Cl- and free water

Often used to treat hypernatremia (because this solution contains a small amount of Na+, it dilutes the plasma sodiumwhile not allowing it to drop too rapidly)

Hypertonic Solutions

5% dextrose in 0.45%

NaCl

A common hypertonic solution used to treat hypovolemia; used to maintain fluid intake

10% dextrose in water

(D10W)

Supplies 340 cal/L

Used for peripheral parenteral nutrition (PPN)

5% dextrose in 0.9%

NaCl (normal saline)

Replaces nutrients and electrolytes

Can temporarily be used to treat hypovolemia if plasma expander is not available

Table 46-11 Complications Associated With Intravenous Infusions



Complication/Cause Signs and Symptoms Nursing Considerations

Infiltration: the escape of fluid into the

subcutaneous tissue Dislodged needlePenetrated vessel wall

Swelling, pallor, coldness, or pain around the

infusion site; significant decrease in the flowrate

Check the infusion site several times

per shift for symptoms.Discontinue the infusion if symptoms

occur.Restart the infusion at a different site.

Limit the movement of the extremity

with the IV.

Sepsis: microorganisms invade the

bloodstream through the catheter insertion

site

Poor insertion technique Multilumen

catheters

Long-term catheter insertion

Frequent dressing changes

Red and tender insertion site Fever, malaise,

other vital sign changes

Assess catheter site daily.

Notify physician immediately if any

signs of infection.

Follow agency protocol for culture of

drainage.

Use scrupulous aseptic technique when

starting an infusion.

Phlebitis: an inflammation of a vein

Mechanical trauma from needle or catheter

Chemical trauma from solution

Septic (due to contamination)

Local, acute tenderness; redness, warmth,

and slight edema of the vein above the

insertion site

Discontinue the infusion immediately.

Apply warm, moist compresses to the

affected site.

Avoid further use of the vein.

Restart the infusion in another vein.

Thrombus: a blood clot Tissue trauma from

needle or catheter

Symptoms similar to phlebitis IV fluid flow

may cease if clot obstructs needle

Stop the infusion immediately.

Apply warm compresses as ordered by

the physician.

Restart the IV at another site.

Do not rub or massage the affected are

Speed shock: the body's reaction to a

substance that is injected into the

circulatory system too rapidly

Too rapid a rate of fluid infusion intocirculation

Pounding headache, fainting, rapid pulse

rate, apprehension, chills, back pains, and

dyspnea

If symptoms develop, discontinue the

infusion immediately.

Report symptoms of speed shock to the

physician immediately.Monitor vital signs if symptoms

develop.

Use the proper IV tubing.

Carefully monitor the rate of fluid flow

Check the rate frequently for accuracy

A time tape is useful for this purpose.

Fluid overload: the condition caused when

too large a volume of fluid infuses into the

circulatory system

Too large a volume of fluid infused into

circulation

Engorged neck veins, increased blood

pressure, and difficulty in breathing

(dyspnea)

If symptoms develop, slow the rate of

infusion.

Notify the physician immediately.

Monitor vital signs.

Carefully monitor the rate of fluid flow

Check the rate frequently for accuracy



Air embolus: air in the circulatory system

Break in the IV system above the heart

level allowing air in the circulatory systemas a bolus

Respiratory distress

Increased heart rate

CyanosisDecreased blood pressure

Change in level of consciousness

Pinch off catheter or secure system to

prevent entry of air.

Place patient on left side inTrendelenburg position.

Call for immediate assistance.Monitor vital signs and pulse oximetry

Documents

Fluid & Electrylyte tables