fluids and electrolytes disturbances

Hypovolemia (FVD)

- Loss of ECF volume is greater than intake of fluid.

• Water and electrolytes are lost in the same proportion.

• This should not be confused with Dehydration which refers

to loss of water ALONE, with increased serum sodium levels

• FVD results from loss of body fluids; occurs more rapidly

with decreased fluid intake.

causes of FVD

- Decreased intake

• GI Losses: Vomiting/Diarrhea/GI Suctioning

• Excess Sweating/Fever

• Burns

• Third-Space Fluid Shifts

Blood Loss

risk factors of FVD

• Diabetes Insipidus (deficit in ADH)

• Adrenal Insufficiency

• Diuresis

• Hemorrhage

• Uncontrolled Diabetes

• Diuretics (Loop diuretics [Furosemide/Lasix])

S/S of FVD

• Acute (rapid) weight loss

• ↓ skin turgor

• Oliguria/Concentrated urine

• Postural hypotension/dizziness

• Prolonged capillary filling time

• Flattened neck veins/Sunken eyes

• Muscle weakness/cramps

• Thirst and confusion

• ↑ Pulse, thready (weak); ↓ BP

- Nausea

- Cool, clammy, pale skin

Labs indicate what for FVD

• ↑ hemoglobin and hematocrit (decreased plasma)

• ↑ serum and urine osmolality and specific gravity

• ↓ urine sodium

- ↑ BUN and creatinine (↑ 20:1 ratio)

- ↑ urine specific gravity and osmolality

Serum electrolyte changes in FVD

• Hypokalemia: Occurs with GI and renal losses as these

organs are major regulators of potassium.

• Hyperkalemia: Adrenal insufficiency due to aldosterone

deficiency causes lack of potassium excretion.

• Hyponatremia: Occurs with increased thirst and ADH

release, which increases water content of the bloodstream.

• Hypernatremia: Can result from increased insensible water

losses and diabetes insipidus.

Medical management of FVD

• Oral route is preferred if deficit is not severe; If acute or

severe, IV route is required.

• Isotonic electrolyte crystalloid solutions (Lactated Ringer’s

or 0.9% sodium chloride) are the first-line choice because

they expand plasma volume.

• When patient becomes normotensive, a hypotonic solution

(0.45% sodium chloride) is used to provide electrolytes and

water for renal excretion of metabolic waste.

Nursing management of FVD

• Fluid I&O is monitored at least every 8 hours, and

sometimes hourly with severe FVD.

• Daily Weights

• Vitals Signs: Observe for weak, rapid pulse and orthostatic

hypotension (safety measures)

• Skin turgor

• Urine Specific gravity

• Mental Status; level of consciousness

Hypervolemia (FVE)

• Expansion of the ECF caused by the abnormal retention

of H2O and Na+ in same proportions as in the ECF.

• FVE can be related to simple fluid overload OR diminished

function of homeostatic mechanisms that regulate fluid.

Contributing factors of FVE

- ↑ dietary sodium; Sodium-containing IV; fluid shifts (burns)

- Hyperaldosteronism

• Heart failure, kidney dysfunction, cirrhosis of the liver

Clinical manifestations of FVE

• Acute weight gain

• Peripheral edema (pitting) and ascites

• Distended jugular veins

• Shortness of breath; wheezing; crackles

• ↑ BP, pulses pressure, CVP

• ↑ bounding pulse and cough; ↑ respiratory rate

• ↑ urine output

Labs indicate what for FVE?

• ↓ hemoglobin and hematocrit

• ↓ serum and urine osmolality

• ↓ urine sodium and specific gravity

serum electrolyte changes in FVE

• Hypokalemia can occur with all diuretics except those that

inhibit aldosterone. Potassium supplements can be taken.

• Hyperkalemia from diuretics that inhibit aldosterone

(potassium-sparing), especially with ↓ renal function.

• Hyponatremia occurs with diuresis due to increased

release of ADH secondary to reduction in volume.

• Hypomagnesium occurs with loop and thiazide diuretics

due to decreased reabsorption and increased excretion.

Medical management of FVE

• Directed at causes: Restricting fluids and sodium or

if related to excessive IV fluids, discontinuing infusion.

• Diuretics: Reduce sodium and water reabsorption

• Dialysis: Kidneys are unable to remove sodium and fluid.

Nursing management of FVE

• Fluid I&O is monitored/Daily Weights

• Assess for Edema

• Monitor diuretics

• Promote fluid restriction/decrease sodium intake

• Promote rest/Skin care, edema=breakdown

• Lung Sounds; Semi-fowler’s position for orthopnea

Sodium (Na+)

• Concentration range 135-145 mEq/L

• Most abundant cation in the ECF

• Major role in water regulation; Water follows sodium.

• Sodium is regulated by renin–angiotensin–aldosterone

system, ADH, and thirst. A loss or gain of sodium is usually

accompanied by a loss or gain of water.

Major functions of sodium

• Maintain blood volume

• Regulate ECF volume, osmolality and distribution

• Muscle contractions

• Transmission of nerve impulses

Hyponatremia

• Serum sodium level less than 135 mEq/L

• Due more to imbalance of water rather than sodium.

causes of hyponatremia

• Adrenal insufficiency

• Water intoxication/dilutional

• SIADH

- Water loss: Vomiting, diarrhea, sweating, diuretics

clinical manifestations of hyponatremia

• poor skin turgor

• dry mucosa

• headache

• decreased salivation

• decreased bp

• nausea

• abdominal cramping

• neurologica changes

Medical management of hyponatremia

Water restriction/Sodium replacement

nursing management of hyponatremia

• Dietary sodium and fluid intake

• Effects of medications (diuretics, lithium)

hypernatremia

• Serum level higher than 145 mEq/L (145 mmol/L).

• Increased serum sodium concentration pulls fluid out of the

cell. This is both an extracellular and an intracellular FVD.

causes of hypernatremia

• Excess water loss

• Excess sodium administration

• Diabetes insipidus

• Heat stroke

• Hypertonic IV solutions

clinical manifestations of hyper natremia

• Thirst

• Dry, swollen tongue

• Sticky mucosa

• Neurologic symptoms*

• Restlessness

• Weakness

medical management of hypernatremia

• Gradual infusion of Hypotonic electrolyte solution or D5W.

nursing management of hypernatremia

• Assess OTC dietary sources of sodium

• Offer and encourage fluid

• Provide sufficient water with tube feedings

foods high in sodium

• AHA recommends no more than 2300 mg/day

• Processed meat and fish: Bacon, lunch meat, sausage,

smoked fish, hot dogs (even turkey)

• Select dairy products: Buttermilk, cheeses, cottage cheese,

ice cream

• Most canned goods: Meats, soups, vegetables

• Processed grains: Dry cereals

• Condiments: BBQ sauce, ketchup, soy sauce, salad dressing

Snack foods: Nuts, popcorn, chips, pretzels

potassium (K+)

• Normal serum concentration ranges from 3.5 to 5 mEq/L;

• Most abundant cation in the ICF; 98% of body’s potassium

is inside the cells; only 2% in ECF.

major functions of potassium

• Maintaining ICF osmolarity

• Transmitting nerve impulses

• Regulating cardiac impulse transmission; Alterations

in K+ can change myocardial irritability and rhythm.

• Skeletal and smooth muscle function

• Regulating acid-base balances

hypokalemia

Serum sodium level less than 3.5 mEq/L

causes of hypokalemia

• GI & Renal Losses (laxative or diuretic abuse)

• Medications (loop diuretics)

• Alterations in acid-base balances (alkalosis)

• Hyperaldosteronism/Cushing’s disease: ↑ Aldosterone

(wastes K+)

• Poor dietary intake

clinical manifestations of hypokalemia

• fatigue

• anorexia, nausea, vomiting

• constipation, abdominal distention. ileus(SBO)

• dysrhythmias

• muscle weakness and cramops (legs)

• paresthesia (tingling and numbness)

• hyporflexia (decrease in DTR)

• polyuria (diluted urine; kidney can’t concentrate)

medical management of hypokalemia

• Increase dietary potassium

• Potassium replacement, IV for severe deficit-

No more than 20 mEq/Hr and up to 80 mEq/L

nursing management of hypokalemia

• Assessment: Sever hypokalemia is life threatening

• Monitor EKG and ABG’s

• K+ supplements (take in divided doses with food or diluted);

avoid K+ supplements with ACE Inhibitors

• Care related to IV K+ administration- K+ is irritating to veins.

• Monitor for digitalis toxicity-↓K+ potentiates digoxin

hyperkalemia

• Serum K+ level greater than 5 mEq/L.

• Seldom occurs in patients with normal renal function.

• Older adults, risk due to ↓ in renin and aldosterone

• Often caused by iatrogenic (treatment-induced) causes.

• Cardiac arrest is more frequently associated with ↑K+

causes of hyperkalemia

• Impaired kidney function/Renal failure (can’t excrete)

• Hypoaldosteronism/Addison’s disease: ↓ Aldosterone

(Na+ loss and K+ retention)

• Excessive intake

• Tissue trauma (burns; tumor lysis): K+ leaks out of cells

• Meds (potassium-sparing diuretics, NSAIDS, ACE inhibitors)

• Acidosis: DKA, Metabolic (H+ “kicks” K+ out of cells)

clinical manifestations of hyperkalemia

• cardiac changes and dysrhythmias (weak pulse decrease in BP)

• Muscle weakness with potential respiratory impairment , muscle twitching (cramps), flaccid paralysis

• paresthesia (pins and needles)

• anxiety; irritability

• GI activity: intestinal colic, nausea, diarrhea

• oliguria( decreased urine output or absent)

medical management of hyperkalemia

• Assessment of serum K+ levels

• Monitor med affects: Potassium-sparing diuretics ↑ K+;

• Furosemide ↓ K+

• Provide sufficient H2O with tube feedings

• Limitation of dietary K+ (salt substitutes)

• Monitor for cardiovascular changes (V-tach, cardiac arrest)

calcium (Ca++)

• Normal serum concentration ranges from 8.8-10.5 mg/dL

• 99% of the body’s calcium is located in the skeletal

system, stored in bones and teeth; 1% is in the serum.

major function of calcium

• Helps to form the bones and teeth.

• Transmitting nerve impulses

• Regulating muscle contractions (heart)

• Blood clotting

• Activating enzymes

hypocalcemia

Serum sodium level less than 8.8 mEq/L

causes of hypocalcemia

• Hypoparathyroidism (and thyroidectomy)

• Malabsorption (diarrhea, Vitamin D, Mg+ deficiency,

• Pancreatitis (excess glucagon secretion=↑ calcitonin)

• Alkalosis

• Massive transfusion of citrated blood (hemorrhage and

shock)-removes Ca++ from the bloodstream

• Renal failure: ↑ serum K+ causes ↓ serum Ca++ levels

• Meds: Antacids (aluminum), caffeine, loop diuretics,

corticosteroids

clinical manifestations of hypocalcemia

• Tetany (most characteristic manifestation)

• numbness, tingling of fingers, toes, and circumoral

• paresthesia

• hyperactive DTR’s; muscle spasms

• (+)Trousseau’s sign/ Chovstek’s sign

• seizures (severe decrease in serum levels)

• bronchospasm: dyspnea, laryngospasm

• abnormal clotting (increased bleeding)

• anxiety, irritability

• weak bones (fractures); dry/brittle hair and nails

medical management of hypocalcemia

• IV calcium gluconate

• Calcium & Vitamin D supplements

• Diet: ↑ Calcium rich foods (1000-1500 mg/day)

nursing management of hypocalcemia

• Assessment: Severe hypocalcemia is life threatening

• Weight bearing exercise to decrease bone calcium loss

• Severe: Seizure precautions, safety if confusion present

• Care related to IV Ca++ administration (digitalis toxicity)

hypercalcemia

• Serum K+ level greater than 10.5 mEq/L.

• Seldom occurs in patients with normal

renal function.

• Older adults, risk due to ↓ in renin and aldosterone

• Often caused by iatrogenic (treatment-induced) causes

• Cardiac arrest is more frequently associated with ↑ K+

causes of hypercalcemia

• Malignancy**

• Hyperparathyroidism (↑ PTH causes release of Ca++ from

bones, and ↑ renal/intestinal absorption)

• Bone loss related to immobility

clinical manifestations of hypercalcemia

(bones, stones, groans, moans, and psychic overtones due to decreased neuromuscular excitability and decreased muscle tone)

• muscle weakness, decreased DTR, lethargy

• incoordination

• intractable N/V, anorexia, constipation

• abdominal cramps and deep bone pain

• polyuria, thirst

• urinary calculi (kidney stones)

• EKG changes, dysrhythmias (V-fib)

Medical management of hypercalcemia

• Treat underlying cause

• Fluids: 3-4 L/day

• Furosemide, phosphates, calcitonin, bisphosphonates, NS

nursing management of hypercalcemia

• Hypercalcemic crisis= ↑ BP, heart block, cardiac arrest

• Encourage ambulation

• Provide fluids containing sodium unless contraindicated

• Fiber for constipation

• Ensure safety- ↑ Ca++ ↑ effects of digitalis

magnesium (Mg+)

• Normal serum concentration ranges from 1.8-3.6 mg/dL

• Abundant intracellular cation and is an activator for many

intracellular enzymes and carb and protein metabolism.

major functions of magnesium

• Relaxation of smooth muscle

• Contraction of skeletal muscle

• Neuromuscular irritability and contractility

• Regulating cardiac function

Hypomagnesia

• Serum sodium level less than 1.8 mEq/L

• Can be due to ↓ K+ & ↓ Ca++

causes of hypomagnesia

• Alcoholism**

• GI losses: NG suction, diarrhea, fistulas

• Hyperparathyroidism, hyperaldosteronism, or

diuretic phase of acute kidney injury

• Enteral or parenteral feeding deficient in Mg+

• Medications (diuretics, digitalis [digoxin toxicity])

• Rapid transfusion of citrated blood

contributing factors of hypomagnesia

• DKA

• Sepsis

• Burns

• Hypothermia

clinical manifestations of hypomagnesia

• neuromuscular irritability (increased deep tendon reflexes)

• muscle weakness and cramps (from increased tightness)

• laryngeal stridor

• positive Trousseau sign and chvosteks sign

• tremors, athetoid movements (ataxia)

• EKG changes and dysrhythmias: torsades de pointes

• Alterations in mood, level of consciousness (seizure precautions), extreme agitation

medical management of hypomagnesia

• Diet (green leafy veggies, nuts) , oral Mg+ supplements

• Magnesium sulfate IV

nursing management of hypomagnesia

• Assessment: Ensure safety (digitalis toxicity)

• Patient teaching: Diet, meds, alcohol use

• Calcium gluconate must be readily available to treat

hypocalcemia tetany or hypermagnesemia

• Dysphagia common (laryngospasm) asses ability to

swallow before admin of food or meds

• Care related to IV Mg+ administration

hypermagnesia

• Serum K+ level greater than 3.6 mEq/L.

• ↑ K+ & ↑ Ca++ are present concurrently

• Rare because kidneys efficiently excrete Mg+.

causes of hypermagnesia

• Renal failure/acute kidney injury (most common cause)

• DKA

• Excessive administration of Magnesium (i.e., preeclampsia)

• ↑ Intake: Tums, Milk of Magnesia

• Lithium intoxication

• Soft tissue injury (trauma, shock, burns)

clinical manifestations of hypermagnesia

• flushing (vasodilation)

• decreased BP (hypotension); AV heart block

• N+V

• hypoactive reflexes (decreased DTR)

• drowsiness

• generalized muscle weakness

• depressed respirations*

• EKG changes, dysrhythmias

medical management of hypermagnesia

• IV Calcium gluconate-antagonizes cardiac effects of Mg+

• Loop diuretics (enhance secretion)

• IV Normal Saline, Lactated Ringers, or Calcium

• Hemodialysis

nursing management of hypermagnesia

• Do not administer medication containing magnesium

• Education: OTC meds with magnesium (milk of magnesia)

• Observe for ↓ DTRs, muscle weakness, and consciousness.

phosphorus(HPO4-)

• Normal serum concentration ranges from 2.5-4.5 mg/dL

• Plentiful in the diet so intake usually exceeds requirements

and kidneys excrete the excess. Primary ICF anion.

major functions

• Essential to function of muscle and RBCs

• Formation of ATP

• Maintenance of Acid-Base balance

• Formation of bones and teeth; regulating Ca++ levels

Hypophosphatemia

Serum sodium level less than 2.5 mEq/L

causes of Hypophosphatemia

• Alcoholism**

• Re-feeding after starvation-stimulates large insulin

release that can shift HPO4

– from ECF to ICF

• Major burns; pain; heat stroke

• Respiratory alkalosis (hyperventilation)

• DKA; hyperparathyroidism

• ↓ Magnesium; ↓ Potassium

• GI Malabsorption: Chronic diarrhea, Crohn’s disease,

Celiac disease, anorexia, bulimia

• Vitamin D deficiency

• Use of diuretics and antacids

clinical manifestations of hypophosphatemia

• decreased ATP impairs cellular energy resources, o2 delivery to tissues, resulting in general weakness and neurological symptoms

• neurologic symptoms; confusion, seizures

• muscle damage/ weakness (diaphram)

• tissue hypoxia

• muscle and bone pain

• acute rhabdomyolysis(skeletal muscle breakdown)

• increased susceptibility to infection

• nystagmus (dancing eyes)

medical management of hypophosphatemia

Oral or IV phosphorous (resulting ↓Ca+

can cause tetany)

hyperphosphatemia

• Serum K+ level greater than 4.5 mEq/L.

• Due to excessive intake, decreased excretion, or disorder

that shifts ICF phosphate into the ECF.

causes of hyperphosphatemia

• Renal Failure from chronic kidney disease/injury

(diminished excretion)-Major cause**

• Hypoparathyroidism

• DKA; Metabolic or respiratory acidosis

• Excessive intake of vitamin D; total parenteral nutrition;

high phosphate intake.

• Chemotherapy (cell lysis)

• Muscle necrosis/rhabdomyolysis

clinical manifestations of hyperphosphatemia

• most symptoms occur due to associated hypocalcemia

• soft tissue calcifications (lung, heart, kidneys, cornea)

• Tetany (severe muscle cramping; most significant)

  Resulting hypocalcemia can cause neuromuscular

  irritability and muscle spasms

  • Tachycardia

medical management of hyperphosphatemia

• With meals: Calcium-binding antacids; phosphate-binding

gels or antacids (amphigel); loop diuretics

• IV Normal Saline

• Dialysis

nursing management of hyperphosphatemia

• Avoid high-phosphorus foods (milk, meat, organs)

• Avoid phosphate-containing laxatives and enemas

• Monitor signs of hypocalcemia (inverse relationship)

chloride(Cl-)

• Normal serum concentration ranges from 98-106 mg/dL

• Cl– is the major anion of the ECF compartment

(found more in interstitial and lymph fluid).

• Likes to hang out with Sodium

• Primarily obtained from the diet as table salt.

major functions of chloride

• Provides H2O balance and maintains acid–base balance.

• Combines with H+ to form hydrochloric acid in the stomach

• Acts as a buffer in O2 and CO2 exchange in RBCs

• Has an inverse relationship with bicarbonate

hypochoremia

Serum sodium level less than 98 mEq/L

causes of hypochloremia

• Addison’s Disease

• Reduced intake or Cl– deficient IV solutions

• GI Losses: GI tube drainage, gastric suctioning, and

severe vomiting and diarrhea

• Excessive sweating, fever, burns

• Meds: Aldosterone, excess diuretics, or laxatives

• DKA (losing urine & electrolytes); Chronic respiratory

acidosis with resulting metabolic alkalosis

clinical manifestations of hypochloremia

• overlap with hyponatremia;s/s=dehydration

• agitation, irritability, twitching, muscle cramps

• weakness, hyperexcitability of muscle, tetany, increased DTR

• dysrhythmias( due to decreased K+)

• seizures, coma (due to decreased Na+)

medical management of hypochloremia

• Replace Chloride: IV NS or 0.45% NS

• discontinue loop, thiazide or osmotic diuretics

nursing management of hypochloremia

• Encourage foods high in Cl- (Salty foods: tomato juice,

canned veggies, processed meats, broth, dates, eggs,

bananas). ↑ Na+ contraindicated CHF, ↑ BP, renal failure

• Avoid free water (without electrolytes)

• Report changes in consciousness, muscle strength and

movement

Hyperchloremia

Serum K+ level greater than 106 mEq/L.

causes of hyperchloremia

• Most common cause: IV induced metabolic acidosis from

↑ Cl– infusions with H2O loss (0.9% NS, 0.45% NS, LR)

• GI: Severe diarrhea (↓ bicarbonate ions).

• Illness: Head trauma, hyperparathyroidism, kidney injury,

dehydration, ↑ perspiration, Hypernatremia, respiratory

alkalosis; metabolic acidosis.

• Meds: Diuretics; ammonium chloride, corticosteroids

clinical manifestations of hyperchloremia

• overlap with metabolic acidosis

• tachypnea; rapid deep respirations

• lethargy; weakness

• hypertension

• cognitive changes ↓

  • Pitting Edema (↑ Cl-

  = ↑ Na+ level = fluid retention)

medical management of hyperchloremia

• Correcting underlying cause and restoring electrolyte, fluid

and acid-base balance are essential: Hypotonic IV,

Lactated Ringer’s (coverts lactate into bicarb in the liver),

IV sodium bicarbonate (↑ renal excretion); diuretics

• Sodium, chloride and fluids are restricted

nursing management of hyperchloremia

Monitor: VS; ABG values; I&O; respiratory, cardiac and

neurologic symptoms