Fluid and Electrolyte Summary

7/27/2019 Fluid and Electrolyte Summary

1/14

Fluid and Electrolyte SummaryFluid Volume

SodiumPotassium

Calcium

MagnesiumOxygen Hemoglobin Dissociation Curve

Extracellular Fluid Volume

Disturbances

1. What is the imbalance?

ECF Volume Disturbance B Excess(Overhydration)

ECF Volume Disturbance B Deficit(Dehydration)

2. What causes the imbalance?

Overloading body with sodium:

Excessive administration of IVfluids, especially hypertonicsolutions

Altered homeostatic regulation of sodiumand water:

Chronic renal failure Congestive heart failure Excessive corticosteroid therapy Syndrome of inappropriate

secretion of ADH (SIADH

Insufficient intake of water and electrolytes:

Impaired thirst mechanism Inability to swallow fluids

Excessive fluid loss through secretions orexcretions:

Potent diuretic therapy Diabetes insipidus Fluid losses from GI tract Excessive sweating

3. What are the signs and symptoms?

Acute weight gain

Peripheral edema

Shortness of breath B rales in lungs

Changes in behaviorB confusion, lethargy,

Acute weight loss

Decreased skin turgor, Dry mucousmembranes, Rough, dry tongue(longitudinal furrows in tongue)

Changes in behaviorB agitation,
http://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#fluidvolumehttp://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#sodiumhttp://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#potassiumhttp://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#calciumhttp://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#magnesiumhttp://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#oxygenhttp://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#tophttp://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#fluidvolumehttp://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#sodiumhttp://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#potassiumhttp://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#calciumhttp://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#magnesiumhttp://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#oxygen


2/14

weakness

Distended neck veins

Full, bounding pulse

Elevated BP

Slow-emptying peripheral veins

Effusions into third spaces

restlessness, weakness

Flat neck veins in supine position

Weak thready pulse

Orthostatic hypotension

Slow-filling peripheral veins

4. What is appropriate clinical nursing care?

Fluid restriction

Dietary Na+ restriction

Diuretic therapy

Since a fluid volume deficit decreasesblood flow to kidneys, treatment mustbegin promptly to prevent damage tokidneys.

If fluids cannot be ingested, isotonic IVfluids (.9% NaCL and D5W) are giveninitially. Electrolytes are added to IVsolution if adequate renal function ispresent (Lactated Ringer=s solution)

Although a fluid volume deficit usuallytakes days to develop, a severe deficitmay occur within hours and may lead tocirculatory collapse (hypovolemic shock)


3/14

Electrolyte Imbalances

Sodium (Na+)1. What is the normal?

Serum Na 135-145 MEq/L

Serum Na+ reflects the osmolality of the blood2. What is the imbalance?

Hypernatremia B Serum Na+ > 145 mEq/L

Serum osmolality > 295 mOsm/kg

Urine s.g. > 1.015

Hyponatremia B Serum Na+ < 135 mEq/L


Increased water loss:

Diabetes insipidus Renal concentrating disorders Watery diarrhea Profuse diaphoresis without fluid

replacementDecreased water intake or increased Na+intake:

Inability to respond to thirst

mechanism Difficulty swallowing fluids Hypertonic tube feedings without

adequate water supplements Excessive administration of

hypertonic NaCl or NaHCO3 Adrenal hyperfunction B

Hyperaldosteronism

Increased water gain (dilutional hyponatremia):

Excessive administration of sodium-

free IV fluids (D5W) Excessive tap water enemas Stimulation of antidiuretic hormone

(ADH) Psychogenic polydipsia

Increased loss of Na+:

Use of hypotonic irrigating solutions

(distilled water) Excessive use of thiazide or loop

diuretics Sodium-losing renal disease Replacement of water, but not

electrolytes lost in massive burns,diaphoresis, vomiting, diarrhea, NGsuction
http://www.austin.cc.tx.us/adnlev2/rnsg1443online/fluid_electrolytes_acid_base/summary_tables.htm#top


4/14

Electrolyte Imbalances

Sodium (Na+) Adrenal insufficiency


Behavioral changes may include:

confusion, lethargy stupor, coma

Extreme thirst

Muscle weakness

Dry, sticky mucous membranes

Behavioral changes may include:

confusion, lethargy convulsions, coma

Muscle weakness

Nausea and abdominal cramps

Postural hypotension


To prevent hypernatremia:

Administer water between hypertonic

tube feedings Teach elderly patients to drink fluids

regularly, as thirst sensation oftendecreases with aging

Offer fluid frequently to patients at

riskTo correct hypernatremia:

Monitor replacement of water loss asprescribed

Diuretics to remove excess Na+ may

also be prescribed Monitor specific gravity of urine

To prevent hyponatremia:

Use normal saline instead of distilled

water for irrigations Avoid tap water enemas in bowel

management Teach patients to replace body fluid

losses with fruit juice or bouillonrather than water

To correct hyponatremia:

Help patient comply with prescribedfluid restriction

Administer hypertonic IV solutions

when prescribed, with great caution


5/14

Potassium (K+)1. What is the normal?

Serum K+ 3.5 - 5.5 mEq/l

K+ is primarily intracellular (98%)


Hyperkalemia B Serum K+ > 5.5 mEq/L

Hypokalemia B Serum K+ < 3.5 mEq/L


Increased K+ intake:

Rapid IV administration of K+ Administration of aged blood Increased oral intake causes

hyperkalemia only ifaccompanied by decreased K+excretion

Excessive use of salt substitutes

(K+ClB)Decreased renal excretion of K+:

Acute and chronic renal failure Decreased production of

Aldosterone Adrenal insufficiency (Addison=s

disease) Excessive use of K+ conserving

diuretics: Spironolactone(Aldactone) and Amiloride(Moduretic)

Movement of K+ into ECF:

Tissue injury (burns, major

surgery, or crush injury) Acidosis B decreased pH with

Decreased K+ intake:

Anorexia nervosa

Gastrointestinal K+ loss:

Vomiting, gastric suction Diarrhea, laxative abuse, recent

ileostomyLarge sweat loss without K+ replacement

Increased renal excretion of K+:

Use of K+ losing diuretics without

K+ replacement Ex.: Furosemide(Lasix), Bumetanide (Bumex), andHCTZ

HyperaldosteronismEntry of K+ into cells:

Alkalosis B increased pH withdecreased H+ in ECF (compensationcauses K+ to shift from ECF to cells)

Hypersecretion of insulin


6/14

Potassium (K+)excess H+ in ECF (compensationcauses K+ to shift from cells to ECF)

Insulin deficiency


Mental confusion GI hyperactivity (N&V, abdominal

cramping and diarrhea) Cardiotoxicity EKG changes (K+ > 6 mEq/L:

o Peaked T waves and

prolongedo

PR interval, wide QRScomplexo Cardiac arrhythmias B

bradycardia and heart blocko Cardiac arrest

Muscle weakness/paralysis,flaccid muscles (lack tone)

Decreased bowel motility

(intestinal ileus, nausea andvomiting)

Polyuria EKG changes (serum K+ < 3

mEq/L):o ST segment depression, T

wave flattening, prominentU waves

o Cardiac arrhythmias BPACs or PVCs

o Respiratory failure B K+


7/14

Potassium (K+) Hypertonic glucose infusion

stimulates release of insulinwhich promotes cellular uptake

of K+ (5-15 units regular insulinwith 50 ml of D50W or 250-500 mlof D10W).

Administer K+ depleting diuretics

as ordered. Administer Kayexalate (cation

exchange resin), if ordered Withhold drugs (e.g., K+ PCN-G)

that contain large amounts of K+ Decrease dietary sources of K+

Administer IV K+ (KCl) in dilutedconcentration. (Usualconcentration 20-40

mEq/L/1000cc. Maximum is80mEq/1000cc.) Never administer potassium

solutions by IV push; doing so willvery likely cause cardiac arrest


8/14

Calcium (Ca++)1. What is the normal?

Serum Ca++ 9-11 mg/dL

Serum Ca++ and serum phosphate vary inversely


Hypercalcemia B Serum Ca++ > 10.5 mg/dL

Hypocalcemia B Serum Ca++ < 8.5 mg/dL


Ca++ release from bone:

Hyperparathyroidism Metastatic carcinoma Multiple myeloma Thyrotoxicosis Prolonged immobilization

Increase GI absorption of Ca++

Excessive ingestion of Vitamin D

Decreased intake or decreased GI absorptionof Ca++:

Vitamin D deficiency Chronic insufficient dietary intake of

Ca++ Acute pancreatitis Overuse of antacids Malabsorption Syndromes

Decrease in physiologically available Ca++:

Hypoparathyroidism Overuse of phosphate-containing

laxatives and enemas (Ex.: FleetPhospho-soda)

Increased urinary excretion of Ca++:

Chronic renal failure



9/14

Calcium (Ca++)Nausea and vomiting

Constipation

Muscle weakness/flaccidity

Depressed deep tendon reflexes

Confusion, lethargy, CNS depression(coma)

Polyuria

Pathological fractures (chronic)

Renal calculi

EKG changes:

Shortened QT interval

Cardiac arrest

Muscle cramps

Confusion, irritability, anxiety

Tetany

Paresthesias of fingers and circumoralregion

Neuromuscular irritability:

Positive Chvostek=s sign B muscle spasm atcheek and corner of mouth in response to tapover facial nerve in front of ear.

Positive Trousseau=s sign B carpal spasmsafter occlusion of blood flow to hand with BPcuff for three minutes.

Hyperactive deep tendon reflexes

Convulsions

EKG changes: Prolonged QT interval

Cardiac arrest


To prevent hypercalcemia:

Increase client mobility

Teach patient to avoid massiveVitamin D supplementation

To correct hypercalcemia:

Administer loop diuretics (Lasix) as

ordered Administer IV normal saline

To prevent hypocalcemia:

Teach patients careful management

of antacids and laxatives Teach patients dietary sources of

calcium and vitamin DTo prevent complications of hypocalcemia:

Administer oral Ca++ supplements


10/14

Calcium (Ca++)(isotonic) as ordered

To prevent complications while correcting

hypercalcemia:

Ensure adequate hydration to

decrease possibility of renal calculiformation

Maintain an acid urine Handle patient gently when

transferring or repositioning toprevent pathological fractures

as ordered Keep 10 ml of 10% IV calcium

gluconate available for emergencyuse after thyroid surgery.Administerslowly, not exceeding 2 ml/min.


11/14

Magnesium (Mg++)1. What is the normal?

Serum Mg++ 1.5-2.5 mEq/L

Mg++ is absorbed primarily through the small intestine2. What is the imbalance?

Hypermagnesemia B Serum Mg++ >2.5 mEq/L Hypomagnesemia B Serum Mg++ < 1.5

mEq/L3. What causes the imbalance?

Excessive intake or absorption of Mg++:

Overuse of antacids containing Mg++ (Maalox,Gelusil, Riopan)

Overuse of laxatives containing Mg++ (Milk ofMagnesia)

Impaired Mg++ excretion:

Advanced renal failure

Adrenal insufficiency (Addison=s disease)

Decreased Mg++ intake or absorption:

Chronic diarrhea

Chronic malnutrition

Malabsorption syndrome B Steatorrhea

Small bowel resection

Chronic alcoholism

Prolonged IV administration without Mg++ supplementation

Gastrointestinal Mg++ loss:

Prolonged diarrhea or nasogastricsuction

Intestinal fistulas

Increased urinary excretion of Mg++:


12/14

Prolonged excessive diuretic therapy4. What are the signs and symptoms?

Hypoactive deep tendon reflexes

Drowsiness, lethargy

Mild hypotension

Nausea and vomiting

Respiratory depression (serum Mg++ > 15

mEq/L)

Cardiac arrhythmias (bradycardia, heart block)

Cardiac arrest (serum Mg++ > 25 mEq/L)

Hyperactive deep tendon reflexes

Coarse tremors

Tetany

Positive Chvostek=s and Trousseau=ssign

Intense confusion

Cardiac arrhythmias (PVC, SVT)

Convulsions

Coma5. What is appropriate clinical nursing care?

To prevent hypermagnesemia:

Teach patients careful management of Mg++containing antacids and laxatives

Teach patients with renal problems to avoidpreparations containing Mg++

To prevent complications and correct hypo-magnesemia safely:

Give fluids to increase urinary output - patientswith impaired renal function will require dialysis

Withhold preparations containing largeamounts of Mg++

Keep 10% calcium gluconate, a magnesiumantagonist, available for emergency use

To prevent hypomagnesemia:

Provide diet counseling for patients atrisk

To correct hypomagnesemia safely:

Administer IM or IV MgSO4 as ordered(20 gms/2ml)

Evaluate renal function beforeadministering Mg++ replacement


13/14

Oxyhemoglobin Dissociation Curve

The oxyhemoglobin dissociation curve explains why a PaO2 of greater than 70mm Hg at rest still allows for an acceptable hemoglobin saturation. Anything lessthan 70 is not compatible with life. These values are to be used when the

patient=

s temperature and acid/base balance are near normal.

On this graph identify the PaO2 for a pulse oximetry reading of

95%

85 %

70%

What action would you take for each of these readings?


14/14

Documents

Fluid and Electrolyte Summary