fluids and electrolytes

Lecture Notes on Fluids and Electrolytes

Prepared By: Mark Fredderick R Abejo R.N, MAN

MS: Fluids and Electrolyte Abejo

STI COLLEGE GLOBAL CITY

College of Nursing

MEDICAL AND SURGICAL NURSING

Fluids and Electrolytes

Lecturer: Mark Fredderick R. Abejo RN, MAN ________________________________________________

FLUIDS & ELECTROLYTES

I. Fluid Status of Human Body

A. Homeostasis: state of the body when

maintaining a state of balance in the presence

of constantly changing conditions

B. Includes balance of fluid, electrolytes, and acid-

base balance

C. Body water intake and output approximately

equal (2500 mL/24 hr.)

Adult body: 40L water, 60% body weight

2/3 intracellular

1/3 extracellular (80% interstitial, 20%

intravascular)

Infant: 70-80% water

Elderly: 40-50% water

II. Body Fluid Composition

A. Water: 60% of body weight

B. Electrolytes: substances that become charged

particles in solution

1. Cations: positively charged (e.g. Na+,

K+)

2. Anions: negatively charged (e.g. Cl-)

3. Both are measured in milliequivalents

per liter (mEq/L)

C. Balance of hydrostatic pressure and osmotic

pressure regulates movement of water

between intravascular and interstitial spaces

III. Body Fluid Distribution:

A. 2 body compartments:

1. Intracellular fluids (ICF): fluids

within cells of body [major

intracellular electrolytes: Potassium

(K+), Magnesium (Mg +2)]

2. Extracellular fluids (ECF): fluid

outside cells; [major extracellular

electrolytes: Sodium (Na+),

Chloride(Cl-)]; this is where

transportation of nutrients, oxygen,

and waste products occurs

B. Locations of ECF:

1. Interstitial: fluid between most cells

2. Intravascular: fluid within blood

vessels; also called plasma

3. Transcellular: fluids of body

including urine, digestive secretion,

cerebrospinal, pleural, synovial,

intraocular, gonadal, pericardial

solute – the substance dissolved

solvent – substance in which the solute is dissolved

- usually water (universal solvent)

molar solution (M) - # of gram-molecular weights of solute

per liter of solution

osmolality – concentration of solute per kg of water

normal range = 275-295 mOsm/kg of water

osmolarity – concentration of solute per L of solution

* since 1kg=1L, & water is the solvent of the human

body, osmolarity & osmolality are used interchangeably

IV. Mechanisms of Body Fluid Movement (i.e. movement

of solutes, solvents across different extracellular

locations)

A. Osmosis: water is mover; water moves from

lower concentration to higher concentration

1. Normal Osmolality of ICF and ECF:

275 – 295 mOsm/kg

2. Types of solutions according to osmolality

Isotonic: all solutions with osmolality

same as that of plasma .Body cells placed

in isotonic fluid: neither shrink nor swell

Hypertonic: fluid with greater

concentration of solutes than plasma

Cells in hypertonic solution: water in

cells moves to outside to equalize

concentrations: cells will shrink

Hypotonic: fluid with lower concentration

of solutes than plasma Cells in hypotonic

solution: water outside cells moves to

inside of cells: cells will swell and

eventually burst (hemolyze)

3. Different intravenous solutions, used to

correct some abnormal conditions,

categorized according to osmolality:

B. Diffusion: solute molecules move from higher

concentration to lower concentration

1. Solute, such as electrolytes, is the

mover; not the water

2. Types: simple and facilitated

(movement of large water-soluble

molecules)

C. Filtration: water and solutes move from area

of higher hydrostatic pressure to lower

hydrostatic pressure

1. Hydrostatic pressure is created by

pumping action of heart and gravity

against capillary wall

2. Usually occurs across capillary

membranes

D. Active Transport: molecules move across

cell membranes against concentration

gradient; requires energy, e.g. Na – K pump

Hydrostatic pressure -pushes fluid out of vessels into tissue

space; higher to lower pressure

– due to water volume in vessels; greater in arterial end

– swelling: varicose veins, fluid overload, kidney failure

& CHF

Osmotic pressure -pulls fluid into vessels; from weaker

concentration to stronger concentration

- from plasma proteins; greater in venous end

- swelling: liver problems, nephrotic syndrome




V. Mechanisms that Regulate Homeostasis:

How the body adapts to fluid and electrolyte changes?

A. Thirst: primary regulator of water intake

(thirst center in brain)

B. Kidneys: regulator of volume and

osmolality by controlling excretion of water

and electrolytes

C. Renin-angiotension-aldosterone

mechanism: response to a drop in blood

pressure; results from vasoconstriction and

sodium regulation by aldosterone

D. Antidiuretic hormone: hormone to

regulate water excretion; responds to

osmolality and blood volume

E. Atrial natriuretic factor: hormone from

atrial heart muscle in response to fluid

excess; causes increased urine output by

blocking aldosterone

Fluid Balance Regulation

Thirst reflex triggered by:

1. decreased salivation & dry mouth

2. increased osmotic pressure stimulates

osmoreceptors in the hypothalamus

3. decreased blood volume activates the

renin/angiontensin pathway, which simulates the

thirst center in hypothalamus

Renin-Angiotensin

1. drop in blood volume in kidneys = renin released

2. renin = acts on plasma protein angiotensin

(released by the liver) to form angiotensin I

3. ACE = converts Angiotensin I to Angiotensin II in

the lungs

4. Angiotensin II = vasoconstriction & aldosterone

release

ADH – produced by hypothalamus, released by posterior

pituitary when osmoreceptor or baroreceptor is

triggered in hypothalamus

Aldosterone – produced by adrenal cortex; promotes Na &

water reabsorption

Sensible & Insensible Fluid Loss

Sensible: urine, vomiting, suctioned secretions

Insensible: lungs , skin, GI and evaporation

Normal Fluid Intake and Loss in Adults

Intake:

Water in food 1,000 mls

Water from oxidation 300 mls

Water in liquid 1,200 mls

TOTAL 2,500 mls

Output:

Skin 500 mls

Lungs 300 mls

Feces 150 mls

Kidneys 1,500 mls

TOTAL 2,500 mls




IV Fluids

Isotonic LR

PNSS (0.9%NSS)

NM

Hypotonic D5W

- isotonic in bag

- dextrose=quickly

metabolized=hypotonic

D2.5W

0.45% NSS

0.3% NSS

0.2% NSS

Hypertonic D50W

D10W

D5NSS

D5LR

3%NSS

Colloids (usually CHONs) & Plasma expanders

Dextran – synthetic polysaccharide, glucose solution

- increase concentration of blood, improving blood

volume up to 24 hrs

- contraindicated: heart failure, pulmonary edema,

cardiogenic shock, and renal failure

Hetastarch – like Dextran, but longer-acting

- expensive

- derived from corn starch

Composition of Fluids

Saline solutions – water, Na, Cl

Dextrose solutions – water or saline, calories

Lactated Ringer‟s – water, Na, Cl, K, Ca, lactate

Plasma expanders – albumin, dextran, plasma protein

(plasmanate) - increases oncotic pressure, pulling fluids

into circulation

Parenteral hyperalimentation – fluid, electrolytes, amino

acids, calories

A. FLUID VOLUME DEFICIT or HYPOVOLEMIA

Definition: This is the loss of extra cellular fluid

volume that exceeds the intake of fluid. The loss of

water and electrolyte is in equal proportion. It can

be called in various terms- vascular, cellular or

intracellular dehydration. But the preferred term is

hypovolemia.

Dehydration refers to loss of WATER alone, with

increased solutes concentration and sodium

concentration

Pathophysiology of Fluid Volume Deficit

Etiologic conditions include:

a. Vomiting

b. Diarrhea

c. Prolonged GI suctioning

d. Increased sweating

e. Inability to gain access to fluids

f. Inadequate fluid intake

g. Massive third spacing

Risk factors are the following:

a. Diabetes Insipidus

b. Adrenal insufficiency

c. Osmotic diuresis

d. Hemorrhage

e. Coma

f. Third-spacing conditions like ascites,

pancreatitis and burns

PATHOPHYSIOLOGY:

Risk Factors --- inadequate fluids in the body ---- decreased

blood volume ----- decreased cellular hydration ---- cellular

shrinkage ---- weight loss, decreased turgor, oliguria,

hypotension, weak pulse, etc.

ASSESSMENT:

Physical examination

Weight loss, tented skin turgor, dry mucus membrane

Hypotension

Tachycardia

Cool skin, acute weight loss

Flat neck veins

Decreased CVP

Subjective cues

Thirst

Nausea, anorexia

Muscle weakness and cramps

Change in mental state

Laboratory findings

1. Elevated BUN due to depletion of fluids or decreased

renal perfusion

2. Hemoconcentration

3. Possible Electrolyte imbalances: Hypokalemia,

Hyperkalemia, Hyponatremia, hypernatremia

4. Urine specific gravity is increased (concentrated

urine) above 1.020

NURSING MANAGEMENT

1. Assess the ongoing status of the patient by doing an

accurate input and output monitoring

2. Monitor daily weights. Approximate weight loss 1

kilogram = 1liter!

3. Monitor Vital signs, skin and tongue turgor, urinary

concentration, mental function and peripheral

circulation

4. Prevent Fluid Volume Deficit from occurring by

identifying risk patients and implement fluid

replacement therapy as needed promptly

5. Correct fluid Volume Deficit by offering fluids orally

if tolerated, anti-emetics if with vomiting, and foods

with adequate electrolytes

6. Maintain skin integrity

7. Provide frequent oral care

8. Teach patient to change position slowly to avoid

sudden postural hypotension




B. FLUID VOLUME EXCESS: HYPERVOLEMIA

Definition : Refers to the isotonic expansion of

the ECF caused by the abnormal retention of

water and sodium

There is excessive retention of water and

electrolytes in equal proportion. Serum sodium

concentration remains NORMAL

Pathophysiology of Fluid Volume Excess

Etiologic conditions and Risks factors

a. Congestive heart failure

b. Renal failure

c. Excessive fluid intake

d. Impaired ability to excrete fluid as in renal

disease

e. Cirrhosis of the liver

f. Consumption of excessive table salts

g. Administration of excessive IVF

h. Abnormal fluid retention

PATHOPHYSIOLOGY

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

increased neck vein distention, tachycardia, hypertension.

The Nursing Process in Fluid Volume Excess

ASSESSMENT

Physical Examination

Increased weight gain

Increased urine output

Moist crackles in the lungs

Increased CVP

Distended neck veins

Wheezing

Dependent edema

Subjective cue/s

Shortness of breath

Change in mental state

Laboratory findings

1. BUN and Creatinine levels are LOW because of

dilution

2. Urine sodium and osmolality decreased (urine

becomes diluted)

3. CXR may show pulmonary congestion

IMPLEMENTATION

ASSIST IN MEDICAL INTERVENTION

1. Administer diuretics as prescribed

2. Assist in hemodialysis

3. Provide dietary restriction of sodium and water

NURSING MANAGEMENT

1. Continually assess the patient‟s condition by

measuring intake and output, daily weight monitoring,

edema assessment and breath sounds

2. Prevent Fluid Volume Excess by adhering to diet

prescription of low salt- foods.

3. Detect and Control Fluid Volume Excess by closely

monitoring IVF therapy, administering medications,

providing rest periods, placing in semi-fowler‟s

position for lung expansion and providing frequent

skin care for the edema

4. Teach patient about edema, ascites, and fluid therapy.

Advise elevation of the extremities, restriction of

fluids, necessity of paracentesis, dialysis and diuretic

therapy.

5. Instruct patient to avoid over-the-counter medications

without first checking with the health care provider

because they may contain sodium

ELECTROLYTES

Electrolytes are charged ions capable of conducting

electricity and are solutes found in all body

compartments.

Sources of electrolytes

Foods and ingested fluids, medications; IVF and

TPN solutions

Functions of Electrolytes Maintains fluid balance

Regulates acid-base balance

Needed for enzymatic secretion and activation

Needed for proper metabolism and effective

processes of muscular contraction, nerve

transmission

Types of Electrolytes

CATIONS- positively charged ions; examples are

sodium, potassium, calcium

ANIONS- negatively charged ions; examples are

chloride and phosphates]

The major ICF cation is potassium (K+); the

major ICF anion is Phosphates

The major ECF cation is Sodium (Na+); the major

ECF anion is Chloride (Cl-)

ELECTROLYTE IMBALANCES

SODIUM

The most abundant cation in the ECF

Normal range in the blood is 135-145 mEq/L

A loss or gain of sodium is usually accompanied by a

loss or gain of water.

Major contributor of the plasma Osmolality

Sources: Diet, medications, IVF. The minimum daily

requirement is 2 grams

Functions:

1. Participates in the Na-K pump

2. Assists in maintaining blood volume

3. Assists in nerve transmission and muscle

contraction

4. Primary determinant of ECF concentration.

5. Controls water distribution throughout the body.

6. Primary regulator of ECF volume.

7. Sodium also functions in the establishment of the

electrochemical state necessary for muscle

contraction and the transmission of nerve

impulses.

8. Regulations: skin, GIT, GUT, Aldosterone

increases Na retention in the kidney




SODIUM DEFICIT: HYPONATREMIA

Definition : Refers to a Sodium serum level of less

than 135 mEq/L. This may result from excessive

sodium loss or excessive water gain.

Pathophysiology

Etiologic Factors

a. Fluid loss such as from Vomiting and nasogastric

suctioning

b. Diarrhea

c. Sweating

d. Use of diuretics

e. Fistula

Other factors

a. Dilutional hyponatremia

Water intoxication, compulsive water

drinking where sodium level is diluted

with increased water intake

b. SIADH

Excessive secretion of ADH causing

water retention and dilutional

hyponatremia

PATHOPHYSIOLOGY

Decrease sodium concentration --- hypotonicity of plasma --

- water from the intravascular space will move out and go to

the intracellular compartment with a higher concentration ---

cell swelling --Water is pulled INTO the cell because of

decreased extracellular sodium level and increased

intracellular concentration

The Nursing Process in HYPONATREMIA

ASSESSMENT

Sodium Deficit (Hyponatremia)

Clinical Manifestations

Clinical manifestations of hyponatremia depend on the

cause, magnitude, and rapidity of onset.

Although nausea and abdominal cramping occur, most

of the symptoms are neuropsychiatric and are probably

related to the cellular swelling and cerebral edema

associated with hyponatremia.

As the extracellular sodium level decreases, the

cellular fluid becomes relatively more concentrated and

„pulls” water into the cells.

In general, those patients having acute decline in serum

sodium levels have more severe symptoms and higher

mortality rates than do those with more slowly

developing hyponatremia.

Features of hyponatremia associated with sodium loss

and water gain include anorexia, muscle cramps, and a

feeling of exhaustion.

When the serum sodium level drops below 115 mEq/L

(SI: 115 mmol/L), thee ff signs of increasing

intracranial pressure occurs:

lethargy

Confusion

muscular twitching

focal weakness

hemiparesis

papilledema

convulsions

In summary:


Altered mental status

Vomiting

Lethargy

Muscle twitching and convulsions (if sodium level is

below 115 mEq/L)

Focal weakness

Subjective Cues

Nausea

Cramps

Anorexia

Headache

Laboratory findings

1. Serum sodium level is less than 135 mEq/L

2. Decreased serum osmolality

3. Urine specific gravity is LOW if caused by sodium loss

4. In SIADH, urine sodium is high and specific gravity is

HIGH

IMPLEMENTATION


1. Provide sodium replacement as ordered. Isotonic saline

is usually ordered.. Infuse the solution very cautiously.

The serum sodium must NOT be increased by greater

than 12 mEq/L because of the danger of pontine

osmotic demyelination

2. Administer lithium and demeclocycline in SIADH

3. Provide water restriction if with excess volume

NURSING MANAGEMENT

1. Provide continuous assessment by doing an accurate

intake and output, daily weights, mental status

examination, urinary sodium levels and GI

manifestations. Maintain seizure precaution

2. Detect and control Hyponatremia by encouraging food

intake with high sodium content, monitoring patients

on lithium therapy, monitoring input of fluids like IVF,

parenteral medication and feedings.

3. Return the Sodium level to Normal by restricting water

intake if the primary problem is water retention.

Administer sodium to normovolemic patient and

elevate the sodium slowly by using sodium chloride

solution

SODIUM EXCESS: HYPERNATREMIA

Serum Sodium level is higher than 145 mEq/L

There is a gain of sodium in excess of water or a

loss of water in excess of sodium.

Pathophysiology:

Etiologic factors

a. Fluid deprivation

b. Water loss from Watery diarrhea, fever, and

hyperventilation

c. Administration of hypertonic solution

d. Increased insensible water loss

e. Inadequate water replacement, inability to swallow

f. Seawater ingestion or excessive oral ingestion of salts




Other factors

a. Diabetes insipidus

b. Heat stroke

c. Near drowning in ocean

d. Malfunction of dialysis

PATHOPHYSIOLOGY

Increased sodium concentration --- hypertonic plasma ----

water will move out form the cell outside to the interstitial

space ----- CELLULAR SHRINKAGE ----- then to the

blood ---- Water pulled from cells because of increased

extracellular sodium level and decreased cellular fluid

concentration

The Nursing Process in HYPERNATREMIA

Sodium Excess (Hypernatremia)


primarily neurologic

Presumably the consequence of cellular dehydration.

Hypernatremia results in a relatively concentrated ECF,

causing water to be pulled from the cells.

Clinically, these changes may be manifested by:

o restlessness and weakness in moderate

hypernatremia

o disorientation, delusions, and

hallucinations in severe hypernatremia.

Dehydration (hypernatremia) is often overlooked as the

primary reason for behavioral changes in the elderly.

If hypernatremia is severe, permanent brain damage

can occur (especially in children). Brain damage is

apparently due to subarachnoid hemorrhages that result

from brain contraction.

A primary characteristic of hypernatremia is thirst.

Thirst is so strong a defender of serum sodium levels in

normal people that hypernatremia never occurs unless the

person is unconscious or is denied access to water;

unfortunately, ill people may have an impaired thirst

mechanism. Other signs include dry, swollen tongue and

sticky mucous membranes. A mild elevation in body

temperature may occur, but on correction of the

hypernatremia the body temperature should return to

normal.

ASSESSMENT


Restlessness, elevated body temperature

Disorientation

Dry, swollen tongue and sticky mucous membrane,

tented skin turgor

Flushed skin, postural hypotension

Increased muscle tone and deep reflexes

Peripheral and pulmonary edema

Subjective Cues

Delusions and hallucinations

Extreme thirst

Behavioral changes

Laboratory findings

1. Serum sodium level exceeds 145 mEq/L

2. Serum osmolality exceeds 295 mOsm/kg

3. Urine specific gravity and osmolality INCREASED

or elevated

IMPLEMENTATION

ASSIST IN THE MEDICAL INTERVENTION

1. Administer hypotonic electrolyte solution slowly as

ordered

2. Administer diuretics as ordered

Loop diuretics (thiazides ok)

3. Desmopressin is prescribed for diabetes insipidus

NURSING MANAGEMENT

1. Continuously monitor the patient by assessing

abnormal loses of water, noting for the thirst and

elevated body temperature and behavioral changes

2. Prevent hypernatremia by offering fluids regularly

and plan with the physician alternative routes if oral

route is not possible. Ensure adequate water for

patients with DI. Administer IVF therapy cautiously

3. Correct the Hypernatremia by monitoring the

patient‟s response to the IVF replacement. Administer

the hypotonic solution very slowly to prevent sudden

cerebral edema.

4. Monitor serum sodium level.

5. Reposition client regularly, keep side-rails up, the bed

in low position and the call bell/light within reach.

6. Provide teaching to avoid over-the counter

medications without consultation as they may contain

sodium

POTASSIUM

The most abundant cation in the ICF

Potassium is the major intracellular electrolyte; in fact,

98% of the body‟s potassium is inside the cells.

The remaining 2% is in the ECF; it is this 2% that is

all-important in neuromuscular function.

Potassium is constantly moving in and out of cells

according to the body‟s needs, under the influence of

the sodium-potassium pump.

Normal range in the blood is 3.5-5 mEq/L

Normal renal function is necessary for maintenance of

potassium balance, because 80-90% of the potassium is

excreted daily from the body by way of the kidneys.

The other less than 20% is lost through the bowel and

sweat glands.

Major electrolyte maintaining ICF balance

Sources- Diet, vegetables, fruits, IVF, medications

Functions:

1. Maintains ICF Osmolality

2. Important for nerve conduction and muscle

contraction

3. Maintains acid-base balance

4. Needed for metabolism of carbohydrates, fats and

proteins

5. Potassium influences both skeletal and cardiac muscle

activity.

( For example, alterations in its concentration change

myocardial irritability and rhythm )

6. Regulations: renal secretion and excretion,

* Aldosterone promotes renal excretion

* Acidosis promotes K exchange for hydrogen




POTASSIUM DEFICIT: HYPOKALEMIA

Condition when the serum concentration of potassium

is less than 3.5 mEq/L

Pathophysiology

Etiologic Factors

a. Gastro-intestinal loss of potassium such as

diarrhea and fistula

b. Vomiting and gastric suctioning

c. Metabolic alkalosis

d. Diaphoresis and renal disorders

e. Ileostomy

Other factor/s

a. Hyperaldosteronism

b. Heart failure

c. Nephrotic syndrome

d. Use of potassium-losing diuretics

e. Insulin therapy

f. Starvation

g. Alcoholics and elderly

PATHOPHYSIOLOGY

Decreased potassium in the body impaired nerve

excitation and transmission signs/symptoms such as

weakness, cardiac dysrhythmias etc..

The Nursing Process in Hypokalemia


Potassium deficiency can result in widespread

derangements in physiologic functions and especially

nerve conduction.

Most important, severe hypokalemia can result in death

through cardiac or respiratory arrest.

Clinical signs rarely develop before the serum

potassium level has fallen below 3 mEq/L (51: 3

mmol/L) unless the rate of fall has been rapid.

Manifestations of hypokalemia include fatigue,

anorexia, nausea, vomiting, muscle weakness,

decreased bowel motility, paresthesias, dysrhythmias,

and increased sensitivity to digitalis.

If prolonged, hypokalemia can lead to impaired renal

concentrating ability, causing dilute urine, polyuria,

nocturia, and polydipsia

ASSESSMENT

Physical examination

Muscle weakness

Decreased bowel motility and abdominal distention

Paresthesias

Dysrhythmias

Increased sensitivity to digitalis

Subjective cues

Nausea , anorexia and vomiting

Fatigue, muscles cramps

Excessive thirst, if severe

Laboratory findings

1. Serum potassium is less than 3.5 mEq/L

2. ECG: FLAT “T” waves, or inverted T waves,

depressed ST segment and presence of the “U” wave

and prolonged PR interval.

3. Metabolic alkalosis

IMPLEMENTATION

ASSIST IN THE MEDICAL INTERVENTION

1. Provide oral or IV replacement of potassium

2. Infuse parenteral potassium supplement. Always dilute

the K in the IVF solution and administer with a pump.

IVF with potassium should be given no faster than 10-

20-mEq/ hour!

3. NEVER administer K by IV bolus or IM

NURSING MANAGEMENT

1. Continuously monitor the patient by assessing the

cardiac status, ECG monitoring, and digitalis

precaution

2. Prevent hypokalemia by encouraging the patient to eat

potassium rich foods like orange juice, bananas,

cantaloupe, peaches, potatoes, dates and apricots.

3. Correct hypokalemia by administering prescribed IV

potassium replacement. The nurse must ensure that the

kidney is functioning properly!

4. Administer IV potassium no faster than 20 mEq/hour

and hook the patient on a cardiac monitor. To

EMPHASIZE: Potassium should NEVER be given IV

bolus or IM!!

5. A concentration greater than 60 mEq/L is not advisable

for peripheral veins.

POTASSIUM EXCESS: HYPERKALEMIA

Serum potassium greater than 5.5 mEq/L

Pathophysiology

Etiologic factors

a. Iatrogenic, excessive intake of potassium

b. Renal failure- decreased renal excretion of

potassium

c. Hypoaldosteronism and Addison‟s disease

d. Improper use of potassium supplements

Other factors

1. Pseudohyperkalemia- tight tourniquet and

hemolysis of blood sample, marked leukocytosis




2. Transfusion of “old” banked blood

3. Acidosis

4. Severe tissue trauma

PATHOPHYSIOLOGY

Increased potassium in the body ---- Causing irritability of

the cardiac cells --- Possible arrhythmias!!

The Nursing Process in Hyperkalemia


By far the most clinically important effect of

hyperkalemia is its effect on the myocardium.

Cardiac effects of an elevated serum potassium level

are usually not significant below a concentration of 7

mEq/L (SI: 7 mmol/L), but they are almost always

present when the level is 8 mEq/L (SI: 8 mmol/L) or

greater.

As the plasma potassium concentration is increased,

disturbances in cardiac conduction occur.

The earliest changes, often occurring at a serum

potassium level greater than 6 mEq/ L (SI: 6

mmol/L), are peaked narrow T waves and a shortened

QT interval.

If the serum potassium level continues to rise, the PR

interval becomes prolonged and is followed by

disappearance of the P waves.

Finally, there is decomposition and prolongation of

the QRS complex. Ventricular dysrhythmias and

cardiac arrest may occur at any point in this

progression.

Note that in Severe hyperkalemia causes muscle

weakness and even paralysis, related to a

depolarization block in muscle.

Similarly, ventricular conduction is slowed.

Although hyperkalemia has marked effects on the

peripheral neuromuscular system, it has little effect on

the central nervous system.

Rapidly ascending muscular weakness leading to

flaccid quadriplegia has been reported in patients with

very high serum potassium levels.

Paralysis of respiratory muscles and those required for

phonation can also occur.

Gastrointestinal manifestations, such as nausea,

intermit tent intestinal colic, and diarrhea, may occur

in hyperkalemic patients.

ASSESSMENT


Diarrhea

Skeletal muscle weakness

Abnormal cardiac rate

Subjective Cues

Nausea

Intestinal pain/colic

Palpitations

Laboratory Findings

1. Peaked and narrow T waves

2. ST segment depression and shortened QT interval

3. Prolonged PR interval

4. Prolonged QRS complex

5. Disappearance of P wave

6. Serum potassium is higher than 5.5 mEq/L

7. Acidosis

IMPLEMENTATION


1. Monitor the patient‟s cardiac status with cardiac

machine

2. Institute emergency therapy to lower potassium level

by:

a. Administering IV calcium gluconate-

antagonizes action of K on cardiac conduction

b. Administering Insulin with dextrose-causes

temporary shift of K into cells

c. Administering sodium bicarbonate-alkalinizes

plasma to cause temporary shift

d. Administering Beta-agonists

e. Administering Kayexalate (cation-exchange

resin)-draws K+ into the bowel

NURSING MANAGEMENT

1. Provide continuous monitoring of cardiac status,

dysrhythmias, and potassium levels.

2. Assess for signs of muscular weakness, paresthesias,

nausea

3. Evaluate and verify all HIGH serum K levels

4. Prevent hyperkalemia by encouraging high risk patient

to adhere to proper potassium restriction

5. Correct hyperkalemia by administering carefully

prescribed drugs. Nurses must ensure that clients

receiving IVF with potassium must be always

monitored and that the potassium supplement is given

correctly

6. Assist in hemodialysis if hyperkalemia cannot be

corrected.

7. Provide client teaching. Advise patients at risk to avoid

eating potassium rich foods, and to use potassium salts

sparingly.

8. Monitor patients for hypokalemia who are receiving

potassium-sparing diuretic

CALCIUM

Majority of calcium is in the bones and teeth

Small amount may be found in the ECF and ICF

Normal serum range is 8.5 – 10.5 mg/dL

Sources: milk and milk products; diet; IVF and

medications




Functions:

1. Needed for formation of bones and teeth

2. For muscular contraction and relaxation

3. For neuronal and cardiac function

4. For enzymatic activation

5. For normal blood clotting

Regulations:

1. GIT- absorbs Ca+ in the intestine; Vitamin D helps to

increase absorption

2. Renal regulation- Ca+ is filtered in the glomerulus

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

deposition of calcium in the bones.

Sources: milk, yogurt, cheese, sardines, broccoli, tofu, green leafy

vegetables

HYPOCALCEMIA Low levels of calcium in the blood

Risk Factors

a. Hypoparathyroidism (idiopathic or postsurgical)

b. Alkalosis (Ca binds to albumin)

c. Corticosteroids (antagonize Vit D)

d. Hyperphosphatemia

e. Vit D deficiency

f. Renal failure (vit D deficiency)

Clinical Manifestation Decreased cardiac contractility

Arrhythmia

ECG: prolonged QT interval, lengthened ST

segment

Trousseau’s sign (inflate BP cuff 20mm above

systole for 3 min = carpopedal spasm)

Chvostek’s sign (tap facial nerve anterior to the

ear = ipsilateral muscle twitching)

Tetany

Hyperreflexia, seizures

Laryngeal spasms/stridor

Diarrhea, hyperactive bowel sounds

Bleeding

Collaborative Management 1. Calcium gluconate 10% IV

2. Calcium chloride 10% IV

3. both usually given by Dr, very slowly; venous irritant;

cardiac probs

4. Oral: calcium citrate, lactate, carbonate; Vit D

supplements

5. Diet: high calcium

6. Watch out for tetany, seizures, laryngospasm, resp &

cardiac arrest

7. Seizure precautions




HYPERCALCEMIA

is an elevated calcium level in the blood

usually from bone resorption

Risk Factors / Causes

a. Hyperparathyroidism (eg adenoma)

b. Metastatic cancer (bone resorption as tumor‟s

ectopic PTH effect) – eg. Multiple myeloma

c. Thiazide diuretics (potentiate PTH effect)

d. Immobility

e. Milk-alkali syndrome (too much milk or antacids

in aegs with peptic ulcer)

Clinical Manifestation groans (constipation)

moans (psychotic noise)

bones (bone pain, especially if PTH is elevated)

stones (kidney stones)

psychiatric overtones (including depression and

confusion)

Arrhythmia

ECG: shortened QT interval, decreased ST

segment

Hyporeflexia, lethargy, coma

Collaborative Management

1. If parathyroid tumor = surgery

2. Diet: low Ca, stop taking Ca Carbonate antacids,

increase fluids

3. IV flushing (usually NaCl)

4. Loop diuretics

5. Corticosteroids

6. Biphosphonates, like etidronate (Calcitonin) &

alendronate (Fosamax)

7. Plicamycin (Mithracin) – inhibits bone resorption

8. Calcitonin – IM or intranasal

9. Dialysis (severe case)

10. Watch out for digitalis toxicity

11. Prevent fractures, handle gently

MAGNESIUM

2nd most abundant intracellular cation

50% found in bone, 45% is intracellular

ATP (adenosine triphosphate), the main source of

energy in cells, must be bound to a magnesium ion in

order to be biologically active.

competes with Ca & P absorption in the GI

inhibits PTH

Normal value : 1.5-2.5 mEq/L

Functions:

1. important in maintaining intracellular activity

2. affects muscle contraction, & especially relaxation

3. maintains normal heart rhythm

4. promotes vasodilation of peripheral arterioles

Sources:

green leafy vegetables, nuts, legumes, seafood, whole

grains, bananas, oranges, cocoa, chocolate

HYPOMAGNESEMIA

is an electrolyte disturbance in which there is an

abnormally low level of magnesium in the blood.

Risk Factors and Cause

a. Chronic alcoholism (most common), Alcohol

stimulates renal excretion of magnesium,

b. Inflammatory bowel disease

c. Small bowel resection

d. GI cancer

e. chronic pancreatitis (poor absorption) f. Loop and thiazide diuretic use (the most common

cause of hypomagnesemia)

g. Antibiotics (i.e. aminoglycoside, amphotericin,

pentamidine, gentamicin, tobramycin, viomycin)

block resorption in the loop of Henle.

h. Excess calcium

i. Excess saturated fats

j. Excess coffee or tea intake

k. Excess phosphoric or carbonic acids (soda pop)

l. Insufficient water consumption

m. Excess salt or sugar intake

n. Insufficient selenium,vitamin D, sunlight

exposure or vitamin B6

o. Increased levels of stress

Clinical Manifestation Weakness

muscle cramps

cardiac arrhythmia

increased irritability of the nervous system with

tremors, athetosis, jerking, nystagmus and an

extensor plantar reflex. Confusion

disorientation

hallucinations

depression

epileptic fits

hypertension, tachycardia and tetany.

* Like hypocalcemia, hypokalemia

Potentiates digitalis toxicity

Collaborative Management 1. Magnesium sulfate IV, IM (make sure renal

function is ok) – may cause flushing

2. Oral: Magnesium oxide 300mg/day,

3. Mg-containing antacids (SE diarrhea)

4. Diet: high magnesium (fruits,green vegetables,

whole grains cereals, milk, meat, nuts and sea

foods )

5. Promotion of safety, protect from injury

HYPERMAGNESEMIA

Etiologic Factors a. Magnesium treatment for pre-eclampsia

b. Renal failure

c. Diabetic Ketoacidosis

d. Excessive use of Mg antacids/laxatives

PATHOPHYSIOLOGY

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

excitability of muscle

http://en.wikipedia.org/wiki/Coffee

http://en.wikipedia.org/wiki/Tea




Clinical Manifestation Hyporeflexia

Hypotension, bradycardia, arrhythmia

Flushing

Weakness, lethargy, coma

Decreased RR & respiratory paralysis

Loss of DTR‟s

*like hypercalcemia

Collaborative Management 1. Diuretics

2. Stop Mg-containing antacids & enemas

3. IV fluids rehydration

4. Calcium gluconate – (antidote, antagonizes

cardiac & respiratory effects of Mg)

5. Dialysis – if RF

PHOSPHORUS

primary intracellular anion

part of ATP – energy

85% bound with Ca in teeth/bones, skeletal muscle

reciprocal balance with Ca

absorption affected by Vit D, regulation affected by

PTH (lowers P level)

Normal value : 2.5-4.5 mg/dL

Functions:

1. bone/teeth formation & strength

2. phospholipids (make up cell membrane integrity)

3. part of ATP

4. affects metabolism, Ca levels

Sources: red & organ meats (brain, liver, kidney), poultry, fish, eggs,

milk, legumes, whole grains, nuts, carbonated drinks

HYPOPHOSPHATEMIA

Risk Factors

a. Decreased Vit D absorption, sunlight exposure

b. Hyperparathyroidism (increased PTH)

c. Aluminum & Mg-containing antacids (bind P)

d. Severe vomiting & diarrhea

Clinical Manifestation Anemia, bruising (weak blood cell membrane)

Seizures, coma

Muscle weakness, paresthesias

Constipation, hypoactive bowel sounds

*Like hypercalcemia


1. Sodium phosphate or potassium phosphate IV

(give slowly, no faster than 10 mEq/hr)

2. Sodium & potassium phosphate orally (Neutra-

Phos, K-Phos) – give with meals to prevent gastric

irritation

3. Avoid Phos-binding antacids

4. Diet: high Mg, milk

5. Monitor joint stiffness, arthralgia, fractures,

bleeding

HYPERPHOSPHATEMIA

Risk Factors a. Acidosis (Ph moves out of cell)

b. Cytotoxic agents/chemotherapy in cancer

c. Renal failure

d. Hypocalcemia

e. Massive BT (P leaks out of cells during storage of

blood)

f. Hyperthyroidism

Clinical Manifestation Calcification of kidney, cornea, heart

Muscle spasms, tetany, hyperreflexia

*like hypocalcemia

Collaborative ManagementM

1. Aluminum antacids as phosphate binders: Al

carbonate (Basaljel), Al hydroxide (Amphojel)

2. Ca carbonate for hypocalcemia

3. Avoid phosphate laxatives/enemas

4. Increase fluid intake

5. Diet: low Phos, no carbonated drinks

CHLORIDE

extracellular anion, part of salt

binds with Na, H (also K, Ca, etc)

exchanges with HCO3 in the kidneys (& in RBCs)

Normal value: 95 -108 mEq/L

Functions:

1. helps regulate BP, serum osmolarity

2. part of HCl

3. acid/base balance (exchanges with HCO3)

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

HYPOCHLOREMIA

Risk Factors a. Diuresis

b. Metabolic alkalosis

c. Hyponatremia, prolonged D5W IV

d. Addison‟s

Clinical Manifestation Slow, shallow respirations (met. Alkalosis)

Hypotension (Na & water loss)


1. Administer IV or Oral : KCl, NaCl

2. Diet: high Cl (& usually Na)

HYPERCHLOREMIA

Risk Factors / Cause a. Metabolic acidosis

b. Usually noted in hyperNa, hyperK




Clinical Manifestation Deep, rapid respirations (met. Acidosis)

hyperK, hyperNa S/S

Increased Cl sweat levels in cystic fibrosis

Collaborative Management 1. Diuretics

2. Hypotonic solutions, D5W to restore balance

3. Diet: low Cl (& usually Na)

4. Treat acidosis

Acid-Base Balance Mechanisms

Buffer - prevents major changes in ECF by releasing or

accepting H ions

Buffer mechanism: first line (takes seconds)

1. combine with very strong acids or bases to

convert them into weaker acids or bases

2. Bicarbonate Buffer System

- most important

- uses HCO3 & carbonic acid/H2CO3 - (20:1)

- closely linked with respiratory & renal

mechanisms

3. Phosphate Buffer System

- more important in intracellular fluids, where

concentration is higher

- similar to bicarbonate buffer system, only uses

phosphate

4. Protein Buffer System

- hemoglobin, a protein buffer, promotes

movement of chloride across RBC membrane in

exchange for HCO3

Respiratory mechanism: 2nd line (takes minutes)

1. increased respirations liberates more CO2 =

increase pH

2. decreased respirations conserve more CO2 =

decrease pH

carbonic acid (H2CO3) = CO2 + water

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

1. kidneys secrete H ions & reabsorb bicarbonate ions =

increase blood pH

2. kidneys form ammonia that combines with H ions to

form ammonium ions, which are excreted in the urine

in exchange for sodium ions

Review: Acid-Base Imbalance

pH – 7.35-7.45

pCO2 – measurement of the CO2 pressure that is being

exerted on the plasma

- 35-45mmHg

PaO2- amount of pressure exerted by O2 on the plasma

- 80-100mmHg

SaO2- percent of hemoglobin saturated with O2

Base excess – amount of HCO3 available in the ECF

- -3 to +3

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

Look at the PCO2

Is it up or down?

If it reflects an opposite response as the pH,

then you know that the condition is a

respiratory imbalance

If it does not reflect an opposite response as the

pH - move to step III

Step 3

Look at the HCO3

Does the HCO3 reflect a corresponding

response with the pH

If it does then the condition is a metabolic

imbalance

FACTORS AFFECTING BODY FLUIDS,

ELECTROLYTES AND ACID-BASE BALANCE

AGE

Infants have higher proportion of body water than

adults

Water content of the body decreases with age

Infants have higher fluid turn-over due to immature

kidney and rapid respiratory rate

GENDER AND BODY SIZE

Women have higher body fat content but lesser

water content

Lean body has higher water content

ENVIRONMENT AND TEMPERATURE

Climate and heat and humidity affect fluid balance

DIET AND LIFESTYLE

Anorexia nervosa will lead to nutritional depletion

Stressful situations will increase metabolism,

increase ADH causing water retention and

increased blood volume

Chronic Alcohol consumption causes malnutrition

ILLNESS

Trauma and burns release K+ in the blood

Cardiac dysfunction will lead to edema and

congestion

MEDICAL TREATMENT, MEDICATIONS AND

SURGERY

Suctioning, diuretics and laxatives may cause

imbalances




ACID-BASE BALANCE PROBLEMS

RESPIRATORY ACIDOSIS

pH < 7.35

pCO2 > 45 mm Hg (excess carbon dioxide in the

blood)

Respiratory system impaired and retaining CO2;

causing acidosis

Common Stimuli

a. Acute respiratory failure from airway obstruction

b. Over-sedation from anesthesia or narcotics

c. Some neuromuscular diseases that affect ability to

use chest muscles

d. Chronic respiratory problems, such as Chronic

Obstructive Lung Disease

Signs and Symptoms

Compensation: kidneys respond by generating and

reabsorbing bicarbonate ions, so HCO3 >26 mm Hg

Respiratory: hypoventilation, slow or shallow

respirations

Neuro: headache, blurred vision, irritability,

confusion

Respiratory collapse leads to unconsciousness and

cardiovascular collapse


1. Early recognition of respiratory status and treat

cause

2. Restore ventilation and gas exchange; CPR for

respiratory failure with oxygen supplementation;

intubation and ventilator support if indicated

3. Treatment of respiratory infections with

bronchodilators, antibiotic therapy

4. Reverse excess anesthetics and narcotics with

medications such as naloxone (Narcan)

5. Chronic respiratory conditions

Breathe in response to low oxygen levels

Adjusted to high carbon dioxide level

through metabolic compensation (therefore,

high CO2 not a breathing trigger)

Cannot receive high levels of oxygen, or will

have no trigger to breathe; will develop

carbon dioxide narcosis

Treat with no higher than 2 liters O2 per

cannula

6. Continue respiratory assessments, monitor further

arterial blood gas results

RESPIRATORY ALKALOSIS pH < 7.35

pCO2 < 35 mm Hg.

Carbon dioxide deficit, secondary to

hyperventilation

Common Stimuli

a. Hyperventilation with anxiety from uncontrolled

fear, pain, stress (e.g. women in labor, trauma

victims)

b. High fever

c. Mechanical ventilation, during anesthesia

Signs and Symptoms

Compensation: kidneys compensate by

eliminating bicarbonate ions; decrease in

bicarbonate HCO3 < 22 mm Hg.

Respiratory: hyperventilating: shallow, rapid

breathing

Neuro: panicked, light-headed, tremors, may

develop tetany, numb hands and feet (related to

symptoms of hypocalcemia; with elevated pH

more Ca ions are bound to serum albumin and less

ionized “active” calcium available for nerve and

muscle conduction)

May progress to seizures, loss of consciousness

(when normal breathing pattern returns)

Cardiac: palpitations, sensation of chest tightness


1. Treatment: encourage client to breathe slowly in a

paper bag to rebreathe CO2

2. Breathe with the patient; provide emotional

support and reassurance, anti-anxiety agents,

sedation

3. On ventilator, adjustment of ventilation settings

(decrease rate and tidal volume)

4. Prevention: pre-procedure teaching, preventative

emotional support, monitor blood gases as

indicated

METABOLIC ACIDOSIS

pH <7.35

Deficit of bicarbonate in the blood NaHCO3 <22

mEq/L

Caused by an excess of acid, or loss of

bicarbonate from the body

Common Stimuli

a. Acute lactic acidosis from tissue hypoxia (lactic

acid produced from anaerobic metabolism with

shock, cardiac arrest)

b. Ketoacidosis (fatty acids are released and

converted to ketones when fat is used to supply

glucose needs as in uncontrolled Type 1 diabetes

or starvation)

c. Acute or chronic renal failure (kidneys unable to

regulate electrolytes)

d. Excessive bicarbonate loss (severe diarrhea,

intestinal suction, bowel fistulas)

e. Usually results from some other disease and is

often accompanied by electrolyte and fluid

imbalances

f. Hyperkalemia often occurs as the hydrogen ions

enter cells to lower the pH displacing the

intracellular potassium; hypercalcemia and

hypomagnesemia may occur

Signs and Symptoms

Compensation: respiratory system begins to

compensate by increasing the depth and rate of

respiration in an effort to lower the CO2 in the blood;

this causes a decreased level of carbon dioxide: pCO2

<35 mm HG.

Neuro changes: headache, weakness, fatigue

progressing to confusion, stupor, and coma

Cardiac: dysrhythmias and possibly cardiac arrest from

hyperkalemia

GI: anorexia, nausea, vomiting

Skin: warm and flushed




Respiratory: tries to compensate by hyperventilation:

deep and rapid respirations known as Kussmaul‟s

respirations

Diagnostic test findings:

1. ABG: pH < 7.35, HCO3 < 22

2. Electrolytes: Serum K+ >5.0 mEq/L

3. Serum Ca+2 > 10.0 mg/dL

4. Serum Mg+2 < 1.6 mg/dL


1. Medications: Correcting underlying cause will

often improve acidosis

2. Restore fluid balance, prevent dehydration with

IV fluids

3. Correct electrolyte imbalances

4. Administer Sodium Bicarbonate IV, if acidosis is

severe and does not respond rapidly enough to

treatment of primary cause. (Oral bicarbonate is

sometimes given to clients with chronic metabolic

acidosis) Be careful not to overtreat and put client

into alkalosis

5. As acidosis improves, hydrogen ions shift out of

cells and potassium moves intracellularly.

Hyperkalemia may become hypokalemia and

potassium replacement will be needed.

6. Assessment

Vital signs

Intake and output

Neuro, GI, and respiratory status;

Cardiac monitoring

Reassess repeated arterial blood gases and

electrolytes

METABOLIC ALKALOSIS

pH >7.45

HCO3 > 26 mEq/L

Caused by a bicarbonate excess, due to loss of

acid, or a bicarbonate excess in the body

Common Stimuli

a. Loss of hydrogen and chloride ions through

excessive vomiting, gastric suctioning, or

excessive diuretic therapy Response to

hypokalemia

b. Excess ingestion of bicarbonate rich antacids or

excessive treatment of acidosis with Sodium

Bicarbonate

Signs and Symptoms

Compensation: Lungs respond by decreasing the

depth and rate of respiration in effort to retain carbon

dioxide and lower pH

Neuro: altered mental status, numbness and tingling

around mouth, fingers, toes, dizziness, muscle spasms

(similar to hypocalcemia due to less ionized calcium

levels)

Respiratory: shallow, slow breathing

Diagnostic test findings

1. ABG‟s: pH> 7.45, HCO3 >26

2. Electrolytes: Serum K+ < 3.5 mEq/L

3. Electrocardiogram: as with hypokalemia


1. Correcting underlying cause will often improve

alkalosis

2. Restore fluid volume and correct electrolyte

imbalances (usually IV NaCl with KCL).

3. With severe cases, acidifying solution may be

administered.

4. Assessment

Vital signs

Neuro, cardiac, respiratory assessment

Repeat arterial blood gases and electrolytes

Selected Water and Electrolyte

Solutions

Isotonic Solutions

A. 0.9% NaCl (isotonic, also called NSS)

Na+ 154 mEq/L

Cl- 154 mEq/L

(308 mOsm/L)

Also available with varying concentrations of dextrose (the

most frequent used is a 5% dextrose concentration

An isotonic solution that expands the ECF

volume, used in hypovolemic states, resuscitative

efforts, shock, diabetic ketoacidosis, metabolic

alkalosis, hypercalcemia, mild Na deficit

Supplies an excess of Na and Cl; can cause fluid

volume excess and hyperchloremic acidosis if

used in excessive volumes, particularly in patients

with compromised renal function, heart failure or

edema

Not desirable as a routine maintenance solution,

as it provides only Na and Cl (and these are

provided in excessive amounts)

When mixed with 5% dextrose, the resulting

solution becomes hypertonic in relation to plasma,

and in addition to the above described

electrolytes, provides 170cal/L

Only solution that may be administered with

blood products

B. Lactated Ringer’s solution (Hartmann’s solution)

Na+ 130 mEq/L

K+ 4 mEq/L

Ca++ 3 mEq/L

Cl- 109 mEq/L

Lactate (metabolized to bicarbonate) 28 mEq/L (274

mOsm/L)

Also available with varying concentration of dextrose (the

most common is 5% dextrose)

An isotonic solution that contains multiple

electrolytes in roughly the same concentration as

found in plasma (note that solution is lacking in

Mg++) provides 9 cal/L

Used in the tx of hypovolemia, burns, fluid lost as

bile or diarrhea, and for acute blood loss

replacement

Lactate is rapidly metabolized into HCO3- in the

body. Lactated Ringer‟s solution should not be

used in lactic acidosis because the ability to

convert lactate into HCO3- is impaired in this

disorder.




Not to be given with a pH > 7.5 because

bicarbonates is formed as lactate breaks down

causing alkalosis

Should not be used in renal failure because it

contains potassium and can cause hyperkalemia

Similar to plasma

C. 5% Dextrose in Water (D5W)

No electrolytes

50 g of glucose

An isotonic solution that supplies 170 cal/L and

free water to aid in renal excretion of solutes

Used in treatment of hypernatremia, fluid loss and

dehydration

Should not be used in excessive volumes in the

early post-op period (when ADH secretion is

increased due to stress reaction)

Should not be used solely in tx of fluid volume

deficit, because it dilutes plasma electrolyte

concentrations

Contraindicated in head injury because it may

cause increased intracranial pressure

Should not be used for fluid resuscitation because

it can cause hyperglycemia

Should be used with caution in patients with renal

or cardiac dse because of risk of fluid overload

Electrolyte-free solutions may cause peripheral

circulatory collapse, anuria in pt. with sodium

deficiency and increased body fluid loss

Converts to hypotonic solution as dextrose is

metabolized by body. Overtime D5W without

NaCl can cause water intoxication (ICF vol.

excess bec. solution is hypotonic)

Hypotonic Solutions

D. 0.45% NaCl

half-strength saline)

Na+ 77 mEq/L

Cl- 77 mEq/L

(154 mOsm/L)

Also available with varying concentration of dextrose (the

most common is 5% dextrose)

Provides Na, Cl and free water

Free water is desirable to aid the kidneys in

elimination of solute

Lacking in electrolytes other than Na and Cl

When mixed with 5% dextrose, the solution

becomes slightly hypertonic to plasma and in

addition to the above-described electrolytes

provides 170 cal/L

Used in the tx of hypertonic dehydration, Na and

Cl depletion and gastric fluid loss

Not indicated for third-space fluid shifts or

increased intracranial pressure

Administer cautiously, because it can cause fluid

shifts from vascular system into cells, resulting in

cardiovascular collapse and increased intracranial

pressure

Hypertonic Solutions

E. 3% NaCl (hypertonic saline)

Na+ 513 mEq/L

Cl- 513 mEq/L

(1026 mOsm/L)

Used to increase ECF volume, decrease cellular

swelling

Highly hypertonic solution used only in critical

situations to treat hyponatremia

Must be administered slowly and cautiously,

because it can cause intravascular volume

overload and pulmonary edema

Supplies no calories

Assists in removing ICF excess

F. 5% NaCl (hypertonic solution)

Na+ 855 mEq/L

Cl- 855 mEq/L

(1710 mOsm/L)

Highly hypertonic solution used to treat

symptomatic hyponatremia

Administered slowly and cautiously, because it

can cause intravascular volume overload and

pulmonary edema

Supplies no calories

Colloid Solutions

G. Dextran in NS or 5% D5W

Available in low-molecular-weight (Dextran 40) and high-

molecular-weight (Dextran 70) forms

Colloid solution used as volume/plasma expander

for intravascular part of ECF

Affects clotting by coating platelets and

decreasing ability to clot

Remains in circulatory system up to 24 hours

Used to treat hypovolemia in early shock to

increase pulse pressure, CO, and arterial BP

Improves microcirculation by decreasing RBC

aggregation

Contraindicated in hemorrhage,

thrombocytopenia, renal dse and severe

dehydration

Not a substitute for blood or blood products

fluids and electrolytes

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