August 7 Module 3 Electrolyte Imbalance S PDF

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Module 3 FLUID & ELECTROLYTE (F & E) Electrolyte Imbalances

Overview................................................... 3 Learning Objectives........................................ 3 Description of Electrolytes................................ 4 Electroneutrality..................................... 4 Electrolyte Distribution.............................. 6 Sodium Imbalances.......................................... 6 Sodium Deficit........................................ 8 Sodium Excess......................................... 18 Potassium Imbalances....................................... 25 Potassium Deficit..................................... 29 Potassium Excess...................................... 37 Calcium Imbalances......................................... 48 Calcium Deficit....................................... 53 Calculating Corrected Serum Calcium Level............. 58 Calcium Excess........................................ 65 Magnesium Imbalances....................................... 73 Magnesium Deficit..................................... 75 Magnesium Excess...................................... 83 Phosphorus Imbalances...................................... 90 Phosphorus Deficit.................................... 91 Phosphorus Excess..................................... 97

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Chloride Imbalances........................................ 103 Chloride Deficit...................................... 106 Chloride Excess....................................... 109 Summary of ECF & ICF Electrolytes & their respective functions ................................................. 112 Review Questions........................................... 114 References................................................. 118

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Overview: Understanding patient’s

electrolytes

assessment

2008).Moreover,

more

thorough

and

recognizing

imbalances

accurate

(Lippincott

Williams

and

accurate

knowledge

on

can &

the

make

Wilkins, different

electrolytes in the body, how they work and their functions guides the student nurse’s on the appropriate, safe, ethical, and holistic care in dealing with any electrolyte imbalance/s

his/her client is experiencing.

This

etiology,

module

discusses

the

description,

assessment

findings,

potential nursing diagnoses, medical management, nursing interventions and evaluation of sodium deficiency/excess, potassium deficiency/excess, chloride

deficiency/excess,

calcium

deficiency/excess,

magnesium

deficiency/excess, and phosphorus deficiency/excess. Module Learning Objectives:

After a successful completion of this module, you should be able to:   

  

Outline the regulation of electrolytes & impact of electrolytes imbalances. Discuss the etiological factors that may increase or decrease the electrolytes level in the body. Identify signs and symptoms of hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypochloremia, hyperchloremia, hypocalcemia, hypercalcemia, hypomagnesemia, hypermagnesemia, hypophosphatemia, and hyperphosphatemia. Explain the different medical management for sodium, potassium, calcium, magnesium, phosphorus, and chloride imbalances. Calculate the corrected serum calcium if the serum albumin level is abnormal. Prioritize nursing diagnoses and interventions of clients with hyponatremia, hypernatremia, hypokalemia, hyperkalemia,

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

hypochloremia, hyperchloremia, hypocalcemia, hypercalcemia, hypomagnesemia, hypermagnesemia, hypophosphatemia, and hyperphosphatemia disorders, basing on the assessment findings. Evaluate the effectiveness of the medical and nursing interventions provided which will be then the basis for modifying and improving nursing interventions.

Description Electrolytes in body fluids are active chemicals (cations that carry positive

charges

and

cations in body

anions

that

carry

fluid are sodium,

negative

charges).

potassium, calcium,

The

major

magnesium, and

hydrogen ions. The major anions are chloride, bicarbonate, phosphate, sulfate, and proteinate ions (Hinkle & Cheever, 2018). Balance of Electrolytes/balancing the pluses and minuses



For a homeostatic condition to exist, equal amounts of anions and cations

must

(extracellular

be

present

fluid

on

and

either

side

intracellular

of

the

fluid

cell

compartments)or

positives and negatives balance each other to achieve a electrical

charge,

and

this

balance

is

termed

membrane

neutral

electroneutrality

(Lippincott Williams & Wilkins, 2008; Paradiso, 1999).



Electrolytes will move from one side of the cell membrane to another in an attempt to maintain an electrically neutral state (Paradiso, 1999, P.48).

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Figure 1. Electroneutrality Reference: https://a12.5bc.myftpupload.com/wpcontent/uploads/electroneutrality.jpg?time=1595839158

Electrolyte distribution

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Electrolyte concentrations in the ICF differ from those in the ECF, as reflected in Table below.

Reference: https://www.semanticscholar.org/paper/Alterations-in-Fluids%2CElectrolytes%2C-and-AcidBase/45ad673f9e63a1477b1a6aea3b9f94e0b48bee35/figure/0

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Electrolyte Imbalances SODIUM IMBALANCES Sodium

(Na+)

is

the

most

abundant

electrolyte

in

the

ECF;

it

concentration ranges from 135 to 145 mEq/L (135 to 145 mmol/L), and it is the primary determinant of ECF volume and osmolality. Sodium has a major role in controlling water distribution throughout the body, because it does not easily cross the cell wall membrane and because of its abundance and high concentration in the body. Sodium is regulated by ADH, thirst, and the renin–angiotensin–aldosterone system. A loss or gain of sodium is usually accompanied by a loss or gain of water. Sodium also functions in establishing the electrochemical state necessary for muscle contraction and the transmission of nerve impulses (Sahay & Sahay, 2014).

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Figure 2. Relationship between sodium and water in the body The

syndrome

of

inappropriate

secretion

of

antidiuretic

hormone

(SIADH) may be associated with sodium imbalance. When there is a decrease in the circulating plasma osmolality, blood volume, or blood pressure, arginine

vasopressin

(AVP)

is

released

from

the

posterior

pituitary.

Oversecretion of AVP can cause SIADH. Patients at risk are older adults, those

with

acquired

immune

deficiency

syndrome

(AIDS),

those

on

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mechanical ventilation, and people taking selective serotonin reuptake inhibitors (SSRIs). Sodium Deficit (Hyponatremia) Hyponatremia refers to a serum sodium level that is less than 135 mEq/L (135 mmol/L) (Sahay & Sahay, 2014). Hyponatremia can present as an acute or chronic form. Acute hyponatremia is commonly the result of a fluid overload in a surgical patient. Chronic hyponatremia is seen more frequently

in

patients

outside

the

hospital

setting,

has

a

longer

duration, and has less serious neurological sequelae. Another type of hyponatremia

is

exercised-associated

hyponatremia,

which

is

more

frequently found in women and those of smaller stature. It can occur during extreme temperatures, because of excessive fluid intake before exercise,

or

prolonged

exercise that

results

in

a

decrease

in

serum

sodium (Earhart et al., 2015). Etiology Hyponatremia primarily occurs due to an imbalance of water rather than sodium. The urine sodium value assists in differentiating renal from nonrenal causes of hyponatremia. Low urine sodium occurs as the kidney retains sodium to compensate for nonrenal fluid loss (i.e., vomiting, diarrhea, sweating). High urine sodium concentration is associated with renal salt wasting (i.e., diuretic use). In dilutional hyponatremia, the ECF volume is increased without any edema.

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A deficiency of aldosterone, as occurs in adrenal insufficiency, also predisposes to sodium deficiency. In addition, the use of certain medications, oxcarbazepine [Prozac], acetate

such

as

anticonvulsants

(Trileptal),

sertraline

(DDAVP),

levetiracetam

[Zoloft],

increases

(i.e.,

the

[Keppra]),

paroxetine risk

of

carbamazepine SSRIs

[Paxil]),

hyponatremia

or

[Tegretol], (fluoxetine desmopressin

(Sahay

&

Sahay,

2014). Syndrome of inappropriate antidiuretic hormone (SIADH) secretion is another cause of hyponatremia. SIADH causes excessive release of ADH, which

causes

inappropriate

and

excessive

water

retention,

thereby

disturbing fluid and electrolyte balance. This syndrome is a major cause of low sodium levels. ADH is released when the body doesn’t need it, which results in water retention and sodium excretion (Willis, 2015) (See the flowchart below).

This flowchart shows the events that occur in SIADH secretion.

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Reference: Willis, 2015 Clinical Manifestations Clinical manifestations of hyponatremia depend on the cause, magnitude, and speed with which the deficit occurs.      

Poor skin turgor dry mucosa headache decreased saliva production orthostatic fall in blood pressure nausea, vomiting, and abdominal cramping occur

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Neurologic changes which are probably related to the cellular swelling and cerebral edema associated with hyponatremia include the following:    As

altered mental status status epilepticus Coma serum

osmolality

decreases

because

of

decreased

sodium

concentration, the cellular fluid becomes relatively more concentrated & pulls water into the cells by osmosis (Hinkle & Cheever, 2018; Willis, 2015) (see Figure 3). Thus, cell swelling results (Hinkle & Cheever, 2018) (see figure 4).

Figure 3. Fluid movement in hyponatremia Reference: Willis, 2015

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Figure 4 .Cell swelling Reference: Hinkle & Cheever, 2018

In general, patients with an acute decrease in serum sodium levels have more cerebral edema and higher mortality rates than do those with more

slowly

developing

hyponatremia.

Acute

decreases

in

sodium,

developing in less than 48 hours, may be associated with brain herniation and

compression

of

midbrain

structures.

Chronic

decreases

in

sodium,

developing over 48 hours or more, can occur in status epilepticus and other neurologic conditions. The severity of symptoms increases with the degree of hyponatremia and the speed with which it develops.

Nursing Alert! When

the

serum

sodium

level

decreases

to

less

than

115

mEq/L, signs of increasing intracranial pressure, such as lethargy,

confusion,

muscle

twitching,

focal

weakness,

hemiparesis, papilledema, seizures, and death, may occur.

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Diagnostic Findings   

serum sodium level is less than 135 mEq/L; SIADH – serum sodium level is lower than 100 mEq/L (100 mmol/L) Serum osmolality is also decreased, except in azotemia with the accumulation of toxins

When hyponatremia is due primarily laboratory results are noted:  

to

sodium

loss,

the

following

urinary sodium – less than 20 mEq/L (20 mmol/L) urine specific gravity is low (1.002 to 1.004)

However, when hyponatremia is due to SIADH:

 

urinary sodium content is greater than 20 mEq/L urine specific gravity is usually greater than 1.012

Medical Management The key to treating hyponatremia is an assessment that focuses on the clinical symptoms of the patient and signs of hyponatremia (including laboratory

values).

As

a

general

rule,

treating

the

underlying

the

condition is essential.

Sodium Replacement 

administration of sodium by mouth, nasogastric parenteral route - most common treatment

tube,

or

a

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

lactated Ringer solution or isotonic saline (0.9% sodium chloride) solution may be prescribed- for those who cannot consume sodium



Serum sodium must not be increased by more than 12 mEq/L in 24 hours to avoid neurologic damage due to demyelination (Sahay & Sahay, 2014 as cited in Hinkle & Cheever, 2018).This condition may occur when the serum sodium concentration is overcorrected (exceeding 140 mEq/L) too rapidly or in the presence of hypoxia or anoxia.



The usual daily sodium requirement in adults is approximately 100 mEq, provided there are not excessive losses.

Water Restriction In patients with normal

or excess fluid

volume, hyponatremia

is

usually treated effectively by restricting fluid. However, if neurologic symptoms are severe (e.g., seizures, delirium, coma), or in patients with traumatic brain injury, it may be necessary to administer small volumes of a hypertonic sodium solution with the goal of alleviating cerebral edema. Pharmacologic Therapy AVP

receptor

hyponatremia

by

antagonists stimulating

are free

pharmacologic water

agents

excretion.

that

IV

treat

conivaptan

hydrochloride (Vaprisol) use is limited to the treatment of hospitalized patients. It may be a useful therapy for those patients with moderate to severe symptomatic hyponatremia but is contraindicated in patients with seizures, delirium, or coma, which warrants the use of hypertonic saline. Tolvaptan significant

(Samsca)

is

an

hypervolemic

oral and

medication

euvolemic

indicated

hyponatremia

for that

clinically must

be

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initiated and monitored in the hospital setting (Comerford, 2015; Sahay & Sahay, 2014). Nursing Management 

needs to identify and monitor patients at risk for hyponatremia



monitors I&O



monitors daily body weight



look for confusion in elderly clients (decreased renal function and subsequent inability to excrete excess fluids)  A diminished sense of thirst or loss of access to food or fluids may also contribute to the problem.  Administration of prescribed and OTC medications that cause sodium loss or water retention is the predisposing factor.



Restrict fluid intake as ordered. (Fluid restriction is the primary treatment for dilutional hyponatremia.) Post a sign about fluid restriction in the patient’s room and make sure the staff, the patient, and his family are aware of the restrictions.

Detecting and Controlling Hyponatremia Early

detection

and

treatment

are

necessary

to

prevent

serious

consequences. For patients at risk, the nurse should: 

closely monitor fluid I&O as well as daily body weight



monitor laboratory values (i.e., sodium)



be alert for GI manifestations such as anorexia, nausea, vomiting, and abdominal cramping



be alert for central nervous system changes, such as lethargy, confusion, muscle twitching, and seizures (Neurologic signs are associated with very low sodium levels that have fallen rapidly because of fluid overloading)

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

monitor laboratory tests: serum sodium, urine, sodium, & specific gravity

For a patient with abnormal losses of sodium who can consume a general diet, the nurse: 

encourages foods and hyponatremia such as:

fluids with high

sodium content

to control

 broth made with one beef cube contains approximately 900 mg of sodium  8 oz of tomato juice contains approximately 700 mg of sodium Dietary sources of sodium          

canned soups and vegetables cheese ketchup processed meats table salt salty snack foods seafood pickled foods seasonings such as monosodium glutamate, seasoned salt, and soy sauce baked goods with baking powder and baking soda

Reference: Willis, 2015

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

needs to be familiar with the sodium content of parenteral fluids

If the primary problem is water retention: 

It is safer to restrict fluid intake than to administer sodium. In normovolemia or hypervolemia, administration of sodium predisposes a patient to fluid volume overload.

In severe hyponatremia, the aim of therapy is to elevate the serum sodium level only enough to alleviate neurologic signs and symptoms. 

It is generally recommended that the serum sodium concentration be increased to no greater than 125 mEq/L (125 mmol/L) with a hypertonic saline solution. Nursing Alert! 

When administering fluids to patients with cardiovascular disease, the nurse assesses for signs of circulatory overload (e.g., cough, dyspnea, puffy eyelids, dependent edema, and excess weight gain in 24 hours). The lungs are auscultated for crackles.

Reference: Hinkle & Cheever, 2018 

Use an infusion pump to ensure that the patient receives only the prescribed volume o...