Alterations in fluid balance/ electrolyte imbalances

Body fluid is classified by its location inside or outside of cells. 

Intracellular fluid is found within cells. ICF  is essential for normal cell function, providing a medium for metabolic processes.

Interstitial fluid is located in spaces between most of the cells in the body. 

Intravascular fluid, called plasma, is contained within arteries, veins and capillaries. 

Transcellular fluid includes urine; digestive secretions; perspiration; and cerebrospinal, pleural, synovial, intraocular, gonadal, and pericardal fluids.

Intracellular fluid 40% of total body weight, and Extracellular fluid 20% of total body weight. 

Total body fluid 60% of total body weight

1500 mLs in adults

About 2500 mLs over 24 hours period




Lemone p. 187

135-145 mEq/L

8.5-10 mg/dL

3.5-5.0 mEq/L

1.6-2.6 mg/dL

98-106 mEq/L

22-26 mEq/L

Osmosis is the process by which water moves across a selectively permeable membrane from an area of lower solute concentration to an area of higher concentration. 

**Osmosis is the primary process that controls body fluid movement between ICF and ECF compartments.

Diffusion is the process by which solute molecules move from an area of high solute concentration to an area of low solute concentration to become evenly distributed.

Facilitated diffusion, also called carrier mediated diffusion, allows large water soluble molecules, such as glucose and amino acids, to diffuse across cell membranes. Protein embedded in cell membrane functions as carriers, helping large molecules cross the membrane.

Filtration is the process by which water and dissolved substances (solutes) move from an area of high hydrostatic pressure to an area of low hydrostatic pressure. This usually occurs across capillary membranes. Hydrostatic pressure is created by the pumping action of the heart and gravity against the capillary wall.

Helps maintain intravascular fluid balance and blood pressure. 

A decrease in blood flow or blood pressure to the kidneys stimulates specialized receptors in the juxtaglomerular cells of the nephrons to produce renin, an enzyme. 

Renin converts angiotensinogen (a plasma protein) in the circulating blood into angiotensin I. 

Angiotensin I  travels through the blood stream to the lungs where it is converted to angiotensin II by angiotensin-coverting enzyme (ACE).  

Angiotensis II is a potent vasoconstrictor; it raises blood pressure. It stimulates the thrist mechanism to promote fluid intake and acts directly on the kidneys, causing them to retain sodium and water. Angiotensin II stimulates the adrenal cortex to release aldosterone. 

Aldosterone promotes sodium and water retention in the distal nephron of the kidney, restoring blood volume.

Antidiuretic hormone (ADH), released by the posterior  pituitary gland, regulates water excretion from the kidneys.  Osmoreceptors in the hypothalamus respond to increases in serum osmolality and decreases in blood volume, stimulating ADH production and release.  

ADH acts on the distal tubules of the kidney, making them more permeable to water and thus increasing water reabsorption. With increased water reabsorption, urine output falls, blood volume is restored and serum osmolality drops as the water dilutes body fluids.

• Fluid volume deficit is a decrease in intravascular, interstitial and/or intracellular fluid in the body. 
• Fluid volume deficits may be the result of excessive fluid losses, insufficient fluid intake or failure  of regulatory mechanisms and fluid shifts within the body.

The most common cause of fluid volume deficit is excess loss of GI fluids from vomiting diarrhea, GI suctioning, intestional fistulas, and intestinal drainage. 

Other causes of fluid  losses include diuretics, renal disorders, endocrine disorders, excessive exercise, hot environment, hemorrhage, and chronic abuse of laxatives and/or enemas. 

Other factors involved in inadequate fluid intake include inability to access fluids, inability to request or swallow fluids, oral trauma or altered thrist mechanisms. 

Older adults are at particular risk for FVD

• FVD  can develop slowly or rapidly depending on the type of fluid loss. Loss of extracellular  fluid volume can lead to hypovolemia, decreased circulating blood volume. 
• Electrolytes often are lost along with fluid, resuting isotonic fluid deficit.

Third spacing is a shift of fluid from the vascular space into an area where it is not available to support normal physiologic processes. 

Fluid may also become trapped within soft tissues following trauma or burns. The trapped fluid represents a volume loss and is unavailable for normal physiologic processes. 

**Daily weights maybe be helpful in uncovering third spaced fluids; however due to fluid or weight loss due to disease processes, these gains may be obscured.

Rapid weight loss is a good indicator of FVD. Each liter of body fluid weighs 1kg (2.2lb)  

The severity of the fluid volume deficit can be estimated by the percentage of rapid weight loss: A loss of 2% of body weight represents a mild FVD; 5% moderate FVD, and 8% or greater, severe  FVD.

Oral rehydration is the safest and most effective treatment for fluid volume deficit  in alert patients who are able to take oral fluids. 

Adults require a minimum of 1500ml of fluid per day or approximately 30ml per Kg of body weight is used to calculate fluid requirements for obese patients for maintenance. 

When the fluid deficit is more severe and when electrolytes have also been lost (eg FVD due to vomiting and/or diarrhea, strenous exercise for longer than an hour or two) a carbohydrate/electrolyte solution such as a sports drink, ginger ale or rehydrating solution is more appropriate. These solutions provide sodium, potassium, chloride, and calories to help meet metabolic needs.

FVD: Decreased systolic

Fluid excess: Increased

FVD: Increased 

Fluid excess: Increased

FVD: Decreased

Fluid excess: Increased

FVD: Normal 

Fluid excess: Moist crackles, wheezes

FVD: Flat 

Fluid excess: Distended

FVD: Rare

Fluid excess: dependent

FVD: Loose, poor turgor

Fluid excess: Taut

FVD: Low, concentrated

Fluid excess: maybe low or normal

FVD: High 

Fluid excess: Low

FVD: Loss

Fluid excess: Gain

• 0.9% Saline 
• Lactated Ringers solution 

Nursing implications:

Monitor for fluid overload; if manifestations occur, discontinue fluids and notify the healthcare provider. 

Do not administer lactated Ringers solution to patients with severe liver disease as the liver may be unable to convert the lactate to bicarbonate and the patient maybe become acidotic. Do not administer if the patient has a blood pH of >7.50

• 0.45% saline or 0.25% saline 
• D5W 

Nursing implications: Monitor for inflammation and infiltration at IV insertion site as hypotonic solutions may cause cells to swell and burst, including those at the insertion site; this narrows the lumen of the vein. 

Monitor blood sodium levels 

Do not administer to patients at risk for increased intracranial pressure (eg, head trauma, stroke, neurosurgery). 

Do not administer to patients at risk for third space shifts (burns, trauma, liver disease, malnutrition)

Hypertonic fluids have a tonicity >350mEq/L and include the following: 

• Fluids containing medications
• D5W sodium chloride
• D5W in lactated ringers solution
• Total parental solutions 

Nursing Implications: 


Monitor for inflammation and infiltration at IV insertion site as hypertonic solutions cause swells to shrink, exposing basement membrane of the vein. 

Monitor blood sodium levels

Monitor circulatory overload 

Do not administer to patients with diabetic ketoacidosis or impaired cardiac or kidney function.

• Fluid and solute loset in proportional amounts. Losses are primarily ECF. 
• Isotonic loss is primarily extracellular. It requires extracellular fluid replacement or vascular volume. 

What will the serum osmolality be? Normal

Causes: 

• Hemorrhage
• GI Losses
• Fever/enviromental heat
• Burns
• Diuretics 
• Third spacing

• More water is lost then solute, primarily sodium. FVD with solute excess.
• Fluid loss is both extra and intracellular 
• What will the serum osmolality be? 
•   Elevated osmolality 

• Causes:
• Inadequate intake
• prolonged Isotonic losses
• watery diarrhea (C.Diff, Ulcerative colitis, Crohns Disease) 
• diabetes insipidus
• increased solute intake

• Thirst, early and unreliable 
• Concentrated and low urine output 
• Dry skin, 
• decreased turgor 
• dry mucous membranes 
• sunken eyeballs
• flat neck veins
• poor peripheral filling 
• hypotension
• postural/frank

• Oral/parental replacement 
• Monitor vital signs, LOC and lab 
• Provide comfort measures
• protect from injury
• medications 
• education

Pitting edema, hypertension, vascular overload, shiny tight skin 

Cough, SOB, crackles

• Weight gain
•  
• Elevated B/P, full pulses, brisk refill

High CVP 

lethargy, confusion

Subtract required fluids (eg. ordered IV fluids, fluid used to dilute IV medications)  from total daily allowance 

Divide remaining fluid allowance- Day shift: 50% of total; evening shift-25% to 33% of total; night shift; remainder. 

Explain the fluid restriction to patient and family members. 

Identify preferred fluids and intake pattern of patient. 

Place allowed amounts of fluids in glasses (gives perception of a full glass) 

Offer ice chips (when melted, ice chips approximately half the frozen volume) 

Provide frequent oral care 

Provide sugarless chewing gum (if allowed) to reduce thirst sensation

• Causes: 
• Diuretics
• GI fluid loss 
• Hypotonic tube feeding
• D5W or hypotonic IV fluids
• Diaphoresis 

• S/S: 
• Anorexia
• N&V 
• Lethargy
• Confusion
• Muscle cramps
• twitching
• Seizures
• Na <135mEq/L 

• Treatment: 
• 24 hour urine specimen collection/ 0.9 NaCl  
• Isotonic fluids/ Isotonic Ringers
• Loop diuretics
• Restrict fluids
• Sodium rich foods 
• If IV saline solutions prescribed, administer very slowly, use isotonic saline if fluid restriction not effective 

Comprehensive review NCLEX RN HESI 2013 pg 36.

• Nursing care- Identify persons at risk
• Teach patients how to recognize s/s
• Importance of drinking fluids containing electrolytes at frequent intervals
• Monitor intake and output 
• Wear cool, loose clothing
• Older adults-effects of meds/potential fluid imbalances

• Causes: 
• Water deprivation
• Hypertonic tube feeding
• Diabetes insipidus
• Heat stroke
• hyperventilation 
• watery diarrhea
• renal failure
• cushing syndrome 
• Most serious cause of cellular dehydration seen in brain
• Patients unable to respond to thirst
• --Due to altered mental status
• --Physical disability 

• S/S: 
• Thirst, rough, dry tongue  
• hyperpyrexia, flushed skin 
• Restlessness
• sticky mucous membranes 
• CNS changes, brain cells contract and may tear and bleed--hallucinations
• lethargy
• irritability 
• May lead to seizures, coma and death in severe dehydration
• Na >145 mEq/L

Treatment: 

• Restrict sodium in the diet
• Beware of hidden sodium in foods and medications
• Increase water intake
• May be H20 or IV replacement
• Gradual decrease of serum sodium by infusion of hypotonic solution
• 0.45% NaCl/D5W IV solution
• Diuretics-increase sodium excretion

Excess water loss may occur with 

• Watery diarrhea
• Increased water losses from 
• Fever
• Hyperventilation
• Excessive perspiration
• Massive burns

• Caused by:
• Ingestion of excess salt
• Hypertonic IV solutions
• Patients with diabetes insipidus
• Clients who experience near drowning in seawater
• heatstroke

• Primary focus is prevention
• Identify risk factors
• Teaching patients/ caregivers
• Monitor lab test results
• Reduce risk for potential for hypernatremia
• Monitor and maintain fluid replacement 
• Institute safety precautions

Offer fluids at regular intervals

If unable to maintain adequate fluid intake, may need alternate route for fluid intake

Teach caregivers the importance of providing adequate water intake for clients receive tube feedings

Monitor/maintain fluid replacement with in prescribed limits

Review lab results of Na+

• Monitor neurologic function, include mental status, level consciousness 
• --N&V
• --Headache
• --Hypertension/Bradycardia 
• Safety measures
• Keep bed in lowest position, side rails up
• Airway at bedside
• Keep familiar items at bedside
• Allow family/significant others to remain with client as much as possible

Reducing sodium intake will help the body excrete excess sodium and water

The body needs less than one-tenth of a teaspoon of salt per day. 

Approximately one third of sodium intake comes from salt added to foods during cooking and at the table; one fourth to one third comes from processed foods; and the rest comes from food and water naturally high sodium

Sodium compounds are used in foods as preservatives, leavening agents and flavor enhancers

Many nonprescription drugs such as (analgesics, cough medicine, laxatives, and antacids) as well as toothpastes and mouthwashes contain high amounts of sodium. 

Low sodium salt substitutes are not really sodium free and may contain about half as much sodium as regular salt. 

 Use salt substitutes sparingly; larger amounts often taste bitter instead of salty. 

• The preference for salt will eventually diminish. 
• Salt, monosodium glutamate, baking soda, and baking powder contain substantial amounts of sodium
• READ LABELS!!! 
• In place of salt or salt substitutes, use herbs, spices, lemon juices, vinegar and wine as flavoring when cooking.

• Common Causes:
• Diuretics
• Diarrhea
• Vomiting
• Gastric suction
• Steroid administration
• Hyperaldosteronism
• Amphotericin B
• Bulimia
• Cushing syndrome

• S/S: 
• Fatigue
• Anorexia
• Nausea/Vomiting
• Muscle weakness
• Decreased GI mobility
• Dysrhythmias
• Paresthesia
• Flat T waves on ECG 
• K <3.5mEq/L 

• Treatment: Administer potassium supplements orally or IV. 
• Oral forms of potassium are unpleasant tasting and are irritating to the GI tract (do not give on empty stomach; dilate) 

NEVER give IV bolus; must be well diluted. 

Assess renal status (i.e. urinary output, prior to administering) 

Encourage foods high in potassium (e.g. bananas, oranges, cantalopes, avocados, spinach, potatoes)

• Monitor serum K+ levels
• K+ replacement, PO or IV
• Dietary sources
• Monitor heart rhythm

IV forms of potassium (KCL) 

• DO NOT administer IV push
• DO NOT add to IV fluids already hanging
• Infuse at rate not to exceed 10 mEq/hour
• DO NOT administer undiluted
• Assess IV site frequently
• Always use an infusion pump
• Cardiac monitor if administering high/rapid doses.

• Do not take K+ supplement if taking a K+ sparing diuretic
• Do not chew enteric coated tabs or allow to dissolve in mouth; may affect potency and action of meds
• Take K+ supplement with meals
• Do not use salt substitutes when taking K+ as salt K+ based

• Pathophysiology:
• Impaired renal excretion of potassium is a primary cause of hyperkalemia. Untreated renal failure, adrenal insufficiency (eg, Addisons disease, or inadequate aldosterone production) 
• and medications (such as potassium sparing diuretics, the antimicrobial drug trimethoprim (Trimprex) and some NSAIDs impair potassium excretion by the kidneys. 

Rapid IV administration of potassium or transfusion of aged blood can lead to hyperkalemia. 

A shift  of potassium ions from ICF can occur in acidosis with severe tissue trauma, during chemotherapy, and due to starvation. 

** the most harmful  consequence of hyperkalemia is its effect on cardiac function.

• Manifestations:
• Diarrhea, colic (abdominal cramping),
• anxiety
• paresthesias
• irritability
• muscle tremors 
• twitching 
• As serum potassium levels increase, muscle weakness develops progressing to flaccid paralysis.
• Muscle weakness develops 
• Heart rate slows to a bradycardia 
• Irregular heart rate

Eliminate parenteral potassium from IV infusions and medications

Administer 50% glucose with regular insulin

• Administer cation exchange resin (Kayexalate)
• Monitor ECG.
• Administer calcium gluconate to protect the heart.
• IV loop diuretics may be prescribed
• Renal dialysis may be required

• Changes in laboratory values: 
• Serum sodium level >145mEq/L
• Increased serum osmolality 
• Increased hematocrit and BUN

• Increased ADH:
• Thirst 
• Decreased urine output 
• Increased urine specific gravity

• Intracellular dehydration: Dry skin, dry mucous membranes
• increased tongue furrows
• Decreased salivation

• Hyperosmolality of ECF= Dehydration of brain neurons 
• Headache
• Restlessness
• Seizures
• Coma

• Decreased vascular volume 
• Tachycardia 
• Pulse weak and thready
• Decreased blood pressure
• vascular collapse
• ECG changes

• Nursing care- to return K+ level to normal by taxing underlying cause/avoid additional K+ intake 
• Meds- Ca+gluconate-IV- counter effects on cardiac conduction system 
• Administer regular insulin/glucose-promotes K+uptake by cells 
• Kayexalate-orally or rectally

Pt's at risk-those who use K+ supplements, K+ sparing diuretics

Teach to read all food and dietary supplements carefully 

• Take K+ supplement as ordered
•  
• Maintain adequate fluid intake 

Effects of excess K+ on electrical conduction and contractility heart are priority

Calcium <8.5 mEq/L

• Caused by: inadequate dietary intake of Vitamin D
• Increased excretion, burns, infection, renal failure 
• surgical removal of parathyroid gland

• Lactose intolerance
• Alcoholism
• Decreased sun exposure
• Older adults less active
• Women at risk after menopause
• Medications can interfere with calcium absorption or promote calcium excretion

Common causes of hypocalcemia are hypoparathyroidism resulting from surgery( parathroidectomy, thyroidectomy, radical neck dissection) and acute pancreatitis. In the patient who has undergone surgery, manifestations of hypocalcemia usually occur within the first 24 to 48 hours, but may be delayed. 

Additional causes: electrolyte imbalance such as hypomagnesemia or hyperphosphatemia), alkalosis, malabsorption disorders that interfere with calcium absorption of bowel, inadequate vitamin D (due to lack of sun exposure or malabsorption). Hyperphosphatemia often occurs in acute renal failure with reciprocal hypocalcemia. Massive transfusion of banked blood can lead to hypocalcemia. Citrate added to blood to prevent clotting and as a preservative. When blood is administered faster than the liver can metabolize the citrate, it can bind with calcium temporarily removing ionized calcium from circulation. 

• Many drugs increase the risk for hypocalcemia including:
• Loop diurectics (such as Lasix)
• anticonvulsants (such as phenytoin (Dilantin) and phenobarbital), phosphates including phosphate enemas) and drugs that lower serum magnesium levels such as cisplatin (Platinol).

• extracellular calcium acts to stabilize neuromuscular membranes
• Effect is decreased in hypocalcemia, increasing neuromuscular irritiability 
• Nervous system becomes more excitable, muscle spasms develop
• Heart muscle-dysrhythmias/ ventricular tachycardia and cardiac arrest

• Diarrhea
• Numbness
• Tingling of extremities
• Convulsions
• Positive Trousseau sign 
• Positive Chvosteks sign 
• CA< 8.5mEq/L 
• At risk for tetany 

• Tetany- most serious complication 
• increased anxiety 
• deep tendon reflexes become hyperactive
• numbness and tingling around mouth
• Trousseau's sign, Chvostek's signs

• Airway obstruction
• Respiratory arrest
• Ventricular dysrhythmias
• cardiac arrest
• heart failure
• convulsions

• Administer calcium supplements orally 30 minutes before meals 
• Oral-Caltrate, Tums, Oscal
• IV-Calcium Chloride 
• Dietary sources: 
• Dairy products 
• Canned salmon
• Spinach, broccoli
• Tofu 
• Administer calcium IV slowly: infiltration can cause tissue necrosis 
• Increase calcium intake (dairy products, greens)

Teach all clients that importance of maintaining adequate calcium intake through diet and supplements as needed

Weight bearing exercises, aerobics and weight training exercise regime

Bone density exam in women/men who are at risk for osteoporosis

Hypercalcemia usually results from increased resorption of calcium from the bones. The two most common causes of bone resorption are hyperparathyrodism and malignancies. 

• This causes calcium to be released from bones as well as increased calcium absorption in the intestines and retention of calcium by the kidneys. 
• Hypercalcemia is a common complication of malignancies. 

It may develop as a result of bone destruction by the tumor or due to a hormone like substances produced by the tumor itself.

Prolonged immobilization 

Excess calcium supplementation

• Muscle weakness
• Constipation
• Anorexia
• N&V
• Polyuria
• Polydipsia
• Neurosis
• Dysrhythmias
• Peptic ulcer disease
• Flank pain/Kidney stones
• CNS changes 
• Ca >10.5 mEq/L

Eliminate parenteral calcium 

Administer agents such as calcitonin to reduce calcium 

Avoid calcium based antacids

Renal dialysis may be required.

• IV fluids with diuretics
• IV fluids- isotonic saline 
• Biophosphonates
• Low calcium diet

• Risk for injury
• Digitalis toxicity
• Promote fluid intake
• Caution with potential fractures

*****Remember calcium has a stabilizing or sedative effect on neuromuscular transmission. Therefore, 

Hypocalcemia--> Increased neuromuscular excitability, muscle twitching, spasms and possible tetany 

Hypercalcemia--> Decreased neuromuscular excitability, muscle weakness and fatigue

• Alcoholism
• Malabsorption 
• Diabetic ketoacidosis
• Prolonged gastric suction
• Diuretics
• inadequate intake-diet low in Mg, long term IV therapy without Mg in solution 
• Increased loss: 
• Increased excretion, NG solution

• Anorexia, distention
• Neuromuscular irritability--Hyperactive reflexes
• Seizures
• Tremors 
• Confusion
• Mood changes 
• Depression
• Disorientation
• Mg <1.6 mEq/L

• Administer MgSO4IV or deep IM injection 
• --Need normal renal function
• --watch labs to avoid overcorrection
• --Monitor depressed deep tendon reflexes
• --(indicate too much Mg) 
• --Monitor cardiac rhythm 
• --PO causes diarrhea, is contraindicated

Encourage foods high in magnesium (meats, nuts, legumes, fish and vegetables)

Usually occurs along with low serum potassium and calcium levels

• Primary cause of hypomagnesium: 
• Chronic Alcoholism
• Chronic GI losses

Magnesium greater than 2.6 mg/dl 

• Caused by: chronic renal failure 
• Antacid use 
• OTC laxative use 
• Other meds that contain magnesium
• Renal failure 
• Adrenal insufficiency
• Excess replacement

• Decreased blood pressure 
• Flushing
• Warmth, sweating
• decreased deep tendon reflexes
• flaccid paralysis
• CNS depression
• bradycardia
• depressed respirations
• Drowsiness, lethargy

Mg> 2.6mEq/L

All medications or compounds containing magnesium are withheld 

Patients with renal failure, hemodialysis or peritoneal dialysis used to remove excess magnesium

• Refeeding after starvation 
• Alcohol withdrawal
• Diabetic ketoacidosis
• Respiratory alkalosis

• S/S: Paresthesias
• Intension tremor, paresthesias
• Confusion, stuporous
• Bone pain 
• Joint stiffness
• Bleeding disorders 
• Impaired WBC function
• Seizures
• Muscle pain
• Mental changes
• Cardiomyopathy
• Respiratory failure
• pH<2.0 mEq/L 

• Correct underlying cause
• Administer oral replacement of phosphates with vitamin D.

• Renal failure
• Excess intake of phosphorus
• Excess Vitamin D
• Chemotherapy

• S/S
• Short term: tenany symptoms, muscle weakness, N&V,dysphagia, decreased blood pressure,cardiac dysrhythmias 
• Long term:  phosphorus precipitation of nonosseous sites 

pH >4.5 mEq/L

• Administer aluminum hydroxide with meals to bind phosphorus
• Decrease diet in phosphate
• Monitor electrolytes 

Dialysis may be required if renal failure is underlying cause.

Administer meds orally in divided doses during the day to bind phosphate 

• Medications-phosphorus binding agents
•  
• Calcium acetate