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Fluid and Electrolyte Summary Fluid Volume Sodium Potassium Calcium Magnesium Oxygen 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:

Insufficient intake of water and electrolytes:


Excessive administration of IV fluids, especially hypertonic solutions

Impaired thirst mechanism Inability to swallow fluids

Altered homeostatic regulation of sodium and water:


Excessive fluid loss through secretions or excretions:


Chronic renal failure Congestive heart failure Excessive corticosteroid therapy Syndrome of inappropriate secretion of ADH (SIADH

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 Acute weight loss Decreased skin turgor, Dry mucous membranes, Rough, dry tongue (longitudinal furrows in tongue)

Changes in behavior B confusion, lethargy, Changes in behavior B agitation,

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 decreases blood flow to kidneys, treatment must begin promptly to prevent damage to kidneys. If fluids cannot be ingested, isotonic IV fluids (.9% NaCL and D5W) are given initially. Electrolytes are added to IV solution if adequate renal function is present (Lactated Ringer=s solution) Although a fluid volume deficit usually takes days to develop, a severe deficit may occur within hours and may lead to circulatory collapse (hypovolemic shock)

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


Serum Na 135-145 MEq/L Serum Na+ reflects the osmolality of the blood

2. What is the imbalance?


Hypernatremia B Serum Na+ > 145 mEq/L Hyponatremia B Serum Na+ < 135 mEq/L Serum osmolality > 295 mOsm/kg Urine s.g. > 1.015

3. What causes the imbalance?


Increased water loss:

Increased water gain (dilutional hyponatremia):


Diabetes insipidus Renal concentrating disorders Watery diarrhea Profuse diaphoresis without fluid replacement

Excessive administration of sodiumfree IV fluids (D5W) Excessive tap water enemas Stimulation of antidiuretic hormone (ADH) Psychogenic polydipsia

Decreased water intake or increased Na+ intake:


Increased loss of Na+:


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

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, NG suction

Electrolyte Imbalances Sodium (Na+)

Adrenal insufficiency

4. What are the signs and symptoms?


Behavioral changes may include:

Behavioral changes may include:


confusion, lethargy stupor, coma

confusion, lethargy convulsions, coma

Extreme thirst Muscle weakness Dry, sticky mucous membranes

Muscle weakness Nausea and abdominal cramps Postural hypotension

5. What is appropriate clinical nursing care?


To prevent hypernatremia:

To prevent hyponatremia:

Administer water between hypertonic tube feedings Teach elderly patients to drink fluids regularly, as thirst sensation often decreases with aging Offer fluid frequently to patients at risk

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 bouillon rather than water

To correct hypernatremia:

To correct hyponatremia:

Monitor replacement of water loss as prescribed Diuretics to remove excess Na+ may also be prescribed Monitor specific gravity of urine

Help patient comply with prescribed fluid restriction Administer hypertonic IV solutions when prescribed, with great caution

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


Serum K+ 3.5 - 5.5 mEq/l K+ is primarily intracellular (98%)

2. What is the imbalance?


Hypokalemia B Serum K+ < 3.5 mEq/L Hyperkalemia B Serum K+ > 5.5 mEq/L

3. What causes the imbalance?


Increased K+ intake:

Decreased K+ intake:

Rapid IV administration of K+ Anorexia nervosa Administration of aged blood Gastrointestinal K+ loss: Increased oral intake causes hyperkalemia only if Vomiting, gastric suction accompanied by decreased K+ Diarrhea, laxative abuse, recent excretion ileostomy Excessive use of salt substitutes + B (K Cl )
Large sweat loss without K+ replacement Increased renal excretion of K+:

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 Entry of K+ into cells: (Aldactone) and Amiloride (Moduretic) Alkalosis B increased pH with

Use of K+ losing diuretics without K+ replacement Ex.: Furosemide (Lasix), Bumetanide (Bumex), and HCTZ Hyperaldosteronism

Movement of K+ into ECF:


decreased H+ in ECF (compensation causes K+ to shift from ECF to cells)

Tissue injury (burns, major surgery, or crush injury) Acidosis B decreased pH with

Hypersecretion of insulin

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

Insulin deficiency 4. What are the signs and symptoms?


Mental confusion GI hyperactivity (N&V, abdominal cramping and diarrhea) Cardiotoxicity EKG changes (K+ > 6 mEq/L: o Peaked T waves and prolonged
o o o

PR interval, wide QRS complex

Cardiac arrhythmias B
bradycardia and heart block

Cardiac arrest

Muscle weakness/paralysis, flaccid muscles (lack tone) Decreased bowel motility (intestinal ileus, nausea and vomiting) Polyuria EKG changes (serum K+ < 3 mEq/L): o ST segment depression, T wave flattening, prominent U waves o Cardiac arrhythmias B
PACs or PVCs
o

Respiratory failure B K+
<1.5 mEq/L

5. What is appropriate clinical nursing care?


To prevent hyperkalemia:

To prevent hypokalemia:

Monitor IV infusions of K+ carefully Evaluate renal function before administering K+ intravenously Avoid use of salt substitutes for patients with renal problems Teach patients, particularly those with renal failure, about foods/fluids which are high in K+

Teach patients which foods have high K+ content Teach patients about their diuretics

To correct hypokalemia: To correct hyperkalemia safely:


Give fluids to increase urinary output IV NaHCO3 a base, shifts K+ into cells in exchange for H+.

Watch for signs of digitalis toxicity in patients receiving digitalis preparations Administer K+ supplements as ordered

Potassium (K+) Hypertonic glucose infusion stimulates release of insulin which promotes cellular uptake of K+ (5-15 units regular insulin with 50 ml of D50W or 250-500 ml of 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 diluted concentration. (Usual concentration 20-40 mEq/L/1000cc. Maximum is 80mEq/1000cc.) Never administer potassium solutions by IV push; doing so will very likely cause cardiac arrest

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


Serum Ca++ 9-11 mg/dL Serum Ca++ and serum phosphate vary inversely

2. What is the imbalance?


Hypocalcemia B Serum Ca++ < 8.5 mg/dL Hypercalcemia B Serum Ca++ > 10.5 mg/dL

3. What causes the imbalance?


Ca++ release from bone:

Decreased intake or decreased GI absorption of Ca++:


Hyperparathyroidism Metastatic carcinoma Multiple myeloma Thyrotoxicosis Prolonged immobilization

Increase GI absorption of Ca++

Vitamin D deficiency Chronic insufficient dietary intake of Ca++ Acute pancreatitis Overuse of antacids Malabsorption Syndromes

Excessive ingestion of Vitamin D

Decrease in physiologically available Ca++:


Hypoparathyroidism Overuse of phosphate-containing laxatives and enemas (Ex.: Fleet Phospho-soda)

Increased urinary excretion of Ca++:

Chronic renal failure

4. What are the signs and symptoms?

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

Muscle cramps Confusion, irritability, anxiety Tetany Paresthesias of fingers and circumoral region Neuromuscular irritability:
Positive Chvostek=s sign B muscle spasm at cheek and corner of mouth in response to tap over facial nerve in front of ear. Positive Trousseau=s sign B carpal spasms after occlusion of blood flow to hand with BP cuff for three minutes.

Hyperactive deep tendon reflexes Convulsions EKG changes: Prolonged QT interval Cardiac arrest

Cardiac arrest

5. What is appropriate clinical nursing care?


To prevent hypercalcemia:

To prevent hypocalcemia:

Increase client mobility Teach patient to avoid massive Vitamin D supplementation

Teach patients careful management of antacids and laxatives Teach patients dietary sources of calcium and vitamin D

To correct hypercalcemia: To prevent complications of hypocalcemia:


Administer loop diuretics (Lasix) as ordered Administer IV normal saline

Administer oral Ca++ supplements

Calcium (Ca++) (isotonic) as ordered


To prevent complications while correcting hypercalcemia:

as ordered Keep 10 ml of 10% IV calcium gluconate available for emergency use after thyroid surgery. Administer
slowly, not exceeding 2 ml/min.

Ensure adequate hydration to decrease possibility of renal calculi formation Maintain an acid urine Handle patient gently when transferring or repositioning to prevent pathological fractures

Magnesium (Mg++)

1. What is the normal?


Serum Mg++ 1.5-2.5 mEq/L Mg++ is absorbed primarily through the small intestine

2. What is the imbalance?

Hypermagnesemia B Serum Mg++ >2.5 mEq/L

Hypomagnesemia B Serum Mg++ < 1.5 mEq/L

3. What causes the imbalance?


Excessive intake or absorption of Mg++: Decreased Mg++ intake or absorption:

Overuse of antacids containing Mg++ (Maalox, Chronic diarrhea Gelusil, Riopan) Chronic malnutrition Overuse of laxatives containing Mg++ (Milk of Magnesia) Malabsorption syndrome B Steatorrhea
Impaired Mg++ excretion:

Small bowel resection Chronic alcoholism Prolonged IV administration without Mg+ + supplementation
Gastrointestinal Mg++ loss:

Advanced renal failure Adrenal insufficiency (Addison=s disease)

Prolonged diarrhea or nasogastric suction Intestinal fistulas


Increased urinary excretion of Mg++:

Prolonged excessive diuretic therapy 4. What are the signs and symptoms? Hypoactive deep tendon reflexes Drowsiness, lethargy Mild hypotension Nausea and vomiting Respiratory depression (serum Mg++ > 15 mEq/L) Hyperactive deep tendon reflexes Coarse tremors Tetany Positive Chvostek=s and Trousseau=s
sign

Intense confusion

Cardiac arrhythmias (bradycardia, heart block) Cardiac arrhythmias (PVC, SVT) Cardiac arrest (serum Mg++ > 25 mEq/L) Convulsions Coma 5. What is appropriate clinical nursing care?
To prevent hypermagnesemia: To prevent hypomagnesemia:

Teach patients careful management of Mg++ containing antacids and laxatives Teach patients with renal problems to avoid preparations containing Mg++
To prevent complications and correct hypomagnesemia safely:

Provide diet counseling for patients at risk


To correct hypomagnesemia safely:

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

Evaluate renal function before Give fluids to increase urinary output - patients administering Mg++ replacement
with impaired renal function will require dialysis

Withhold preparations containing large amounts of Mg++ Keep 10% calcium gluconate, a magnesium antagonist, available for emergency use

Oxyhemoglobin Dissociation Curve


The oxyhemoglobin dissociation curve explains why a P aO2 of greater than 70 mm Hg at rest still allows for an acceptable hemoglobin saturation. Anything less than 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?

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