Fluid and Electrolites

Disorders of Fluid & Electrolyte Balance

Class 6 Objectives

 Upon completion of this lesson, the student will be able to

 describe the outcomes associated with hypo and hypervolemia.

 distinguish between the different etiologies of major electrolyte imbalances.

 list the manifestations of electrolyte imbalances.

 identify normal distribution of ICF and ECF.

 state the normal serum values for Na, K, Cl, Mg, PO4 ,Ca.

Fluids

 Distribution of total body water (TBW)

 60% of adult body weight is fluid

Gender, body mass & age considerations

 Intracellular (ICF, within cells = 40% of body weight)

 Extracellular (ECF, plasma, interstitial & lymph =20% of body weight)

 1 Litre water = 2.2lb or 1 kg

Sources and losses of FLUIDS to maintain homeostasis

 Kidneys 1,500 mL/d

 Sensible skin losses100 mL/d

 Insensible losses 350 mL/d

 Lungs 350 mL/d

 GI tract 200mL/d

 Fluid 1,500 mL/d

 Water from foods 750 mL/d

 Water from metabolism 250 mL/d

Starling’s Law of the Capillary

 Fluids leave (filtration) or enter (re-absorption) the capillaries depending on how the pressure in the capillary and interstitial spaces relate to one another

 Volume re-absorbed is similar to volume filtered: “A net equilibrium”

 Regulates relative volumes of blood & interstitial fluid

Capillary Exchange

 The 5% of blood in the systemic capillaries = the bulk of blood that exchanges materials with systemic tissue cells

 Substances that pass through thin capillary walls into interstitial fluid and then into cells are: nutrients & oxygen

 Substances that are secreted by tissue cells and removed from them are: wastes & CO2

Developmental Differences

 Infants & young children

 Four areas of immature functioning

• Increased fluid intake and output relative to size

• Total body fluid is 20% more than adults

• Greater surface area relative to size: > water loss through skin

• Increased metabolic rate up to 2 years

• Immature kidney function

• requires more fluid to excrete wastes

Fluid Shifts

“Third Spacing”

 Excess fluid in interstitial spaces and connective tissues between cells [edema]

OR

 Excess fluid in potential spaces [effusion]

• peritoneal cavity

• pericardial sac

• synovial cavities of joints

• alveoli or intra-pleural spaces

Fluid Shifts

“Third Spacing”

 Etiology

 Caused by an increase in filtration and/or decrease in reabsorption due to altered capillary forces

 Pathophysiology

 Lymph edema

 Angioedema

Mechanisms causing third spacing & edema

 massive inflammation/pancreatitis

 venous obstruction/liver dysfunction

 increased blood volume

 low serum albumin/malnutrition

Hypovolemia

 A decrease in the ECF volume

 Intravascular and interstitial volume

 Isotonic volume deficit may be due to

 Decreased intake of isotonic fluids

 Or excessive loss

• vomiting or diarrhea

• hemorrhage

• urine output

Hypovolemia

 Hematocrit (Hct) is sensitive to fluid shifts

 volume (%) of erythrocytes in whole blood

 40-54 % males

 37-47 % females

 11.2-16.5 % children

 BUN will be elevated d/t < volume

 11-23 mg/dL

 Urine specific gravity above 1.020

Hypovolemia: manifestations

 Decreased tissue perfusion

 Check capillary refill time

 Decreased blood volume

 Hypotension, tachycardia, oliguria

 Tissue dehydration

 Loss of skin turgor/dry skin

 Possible temperature elevation

 Extreme thirst

Hypovolemia

 Nursing Responsibilities:

 calculate I & O frequently

• minimal urinary output = 30cc/hr

• check urine specific gravity

 check O2 saturations

 draw & analyze blood gases

 auscultate lungs (side to side)

 check temperature distal from heart

 give isotonic solutions (oral or IV)

• Normal saline; dextrose, Ringer’s lactate

 give a fluid bolus as ordered

Hypervolemia

 Excess of isotonic fluid in the intravascular and interstitial spaces

 Isotonic fluid retention

• Olguric state r/t renal failure

• Excessive sodium intake (IV or oral)

 Secondary Hyperaldosteronism

• Inappropriate renal reabsorption of water and sodium,and increased renal secretion of potassium

 Iatrogenic hypervolemia/excessive intake

 Abnormal fluid retention d/t CHF or corticosteroid therapy

Hypervolemia

 Patho

 An excess in blood volume results in elevated CHP and third spacing

Clinical manifestations

• Dependent edema/weight gain

• Hypertension

• Bounding pulse

• Oliguria or increased urinary output

Hypervolemia

 Nursing Responsibilities:

 Monitor I & O carefully

 Weigh the patient daily

 Take vital signs q shift and p.r.n.

 Auscultate lungs (side to side); assess lung sounds

 check temperature distal from heart

 Instruct sodium-restricted diet as ordered

 Administer diuretics as prescribed

 Restrict sodium and water as ordered

Hypovolemia & Hypervolemia

Nursing Responsibilities

 Calculate I & O frequently

 Check O2 saturations

 Draw & analyze blood gases

 Auscultate lungs (side to side)

 Check temperature distal from heart

 Give isotonic solutions (oral or IV): Normal saline; dextrose, Ringer’s lactate

 Give a fluid bolus as ordered

 Monitor I & O carefully

 Weigh the patient daily

 Take vital signs q shift and p.r.n.

 Auscultate lungs (side to side); assess lung sounds

 check temperature distal from heart

 Instruct sodium-restricted diet as ordered

 Administer diuretics as prescribed

 Restrict sodium and water as ordered

Major Electrolytes

 Electrolytes

 Na+, K+, Ca++, Mg+ = cations

 HCO-3, Cl-, PO4 = anions

 ICF = K+ and PO4=

 ECF = Na+ and Cl-

 Regulatory Mechanisms:

 osmosis and diffusion

 osmolarity

 capillary dynamics: i.e., hydrostatic pressure

Hyponatremia

(Na+ < 135 mEq/L)

 Low sodium determined by blood chemistry

The most common electrolyte imbalance:

• 2.5% of hospitalized patients

 Sodium supports neuron transmission

 Mechanism and examples

 Free water gain/compulsive H2O drinking

 Deficient sodium intake

 Renal sodium loss in excess of water

 Water in excess of sodium gain/SIADH

 Fluid losses: vomiting, diarrhea, diuretic thx

Hyponatremia

(Na+ < 135 mEq/L)

 Manifestations

 Water excess

 rapid weight gain

 Na+ loss

neurological symptoms

• irritability, seizures, < LOC

 Muscle cramps

 Anorexia/ Nausea/Vomiting (subtle signs)

 Treat water excess

 Fluid restriction (I&O)

Treat sodium loss

• Oral or IV sodium

Hyponatremia:

Nursing Responsibilities

 Monitor intake and output carefully

 Weigh the patient daily

 Assess neurologic and GI status

 Administer sodium supplements as ordered

 Monitor for signs of fluid volume excess

 Maintain seizure precautions

 Restrict fluids as ordered

Hypernatremia

(Na+ >145 mEq/L)

Etiology

 Water loss or sodium gains

 Elderly / or comatose patients/inability to swallow

 Na+ intake > water intake

 Diabetes insipidus (excessive fluid loss)  < production of ADH

 Damage to hypothalamic thirst center?

• Tumor or CVA?

 Manifestations

 Thirst, dry tongue, dry skin

 Restlessness; < LOC; lethargy Coma;

 Weight changes

Hypernatremia

(Na+ >145 mEq/L)

Treatment (Rx)

 Dilute Na+ and promote secretion

 Fluids (5% D/W) and diuretics

 Always check LOC

 loose alertness & orientation

• sepsis, head injury, intracranial bleed

 Sodium pulls fluid to cause blood vessels to burst

Hypernatremia:

Nursing Responsibilities

 Monitor intake and output carefully

 Weigh the patient daily

 Assess vital signs, skin turgor and neurologic status

 Protect the patient from injury

 Encourage fluid intake as appropriate

 Infuse hypotonic solution as ordered

Potassium (K+)

3.5-5.0 mEq/L

 Primarily an intracellular ion; small amount in plasma is essential for normal neuromuscular and cardiac function

 Maintained by the cellular sodium-potassium pump

 K+ changes  altered excitability of muscles

 Eliminated by kidneys

 renal problems causes hyperkalemia

 Insulin: causes K+ to move from ECF  ICF

 Acidosis, trauma to cells, and exercise

• cause K+ to move from ICF  ECF:

Hyperkalemia

K+ > 5.5 mEq/L

 Major Causes

 Increased potassium intake

• excess or rapid delivery of K+

• penicillin containing K+

• Massive blood transfusion with irradiated packed red cells

 Shift of K+ from the ICF to ECF

• Acidosis, uncontrolled DM

• increased cell lysis (e.g. cytotoxic drugs, severe tissue trauma)

 Decreased renal excretion

• Digitalis toxicity, renal failure, overuse of potassium sparing diuretics (spironolactone)

Hyperkalemia

K+ > 5.5 mEq/L

Manifestations:

 weak skeletal muscles/ paralysis > 8 mEq/L

 paresthesias

 irritability

 abdominal cramping with diarrhea

 irregular pulse  EKG changes  cardiac standstill

 EKG changes

• peaked T-waves and a shortened QT interval occur

• Depressed ST segment and widened QRS interval

Hyperkalemia

K+ > 5.5 mEq/L

Management

 Eliminate K+

 Diuretics (Lasix)

 Dialysis

 Kayexalate

 Increased fluids

 IV insulin

 Cardiac monitor

Hyperkalemia:

Nursing Responsibilities

 Teach patients at increased risk for hyperkalemia (such as those with renal failure) to avoid high potassium foods

 Monitor ECG for abnormalities

 Prepare for and assist with aggressive therapy, as ordered, which may include kayexalate, parenteral sodium bicarbonate, parenteral insulin and glucose, dialysis

Hypokalemia

K+ < 3.5 mEq

 Major causes

 < intake of potassium or > cellular uptake of potassium

• Insulin: promotes K+ uptake by muscle & liver cells

• When insulin is given: K+ goes into ICF  < serum K+ level

 Uncontrolled diabetes mellitus:

• > Glucose: osmotic diuretic  > potassium via urinary excretion

• Diabetic Ketoacidosis:  H+ ions in ECF  exchange across cell membranes  K+ is first elevated and then K+ stores are excreted via urine

Hypokalemia

K+ < 3.5 mEq

 Epinephrine: promotes uptake into cells

• stress, acute illness, hypoglycemia

 Excessive GI loss: diarrhea & NG suction  metabolic alkalosis

 Diuretics: Lasix (watch K+ levels)

 Excessive renal excretion of K+  elevated aldosterone  diuresis

Hypokalemia

K+ < 3.5 mEq

 Signs & Symptoms

 Muscle weakness: hypotonia

 Cardiac dysrhytmias (T-wave inversion or PVCs; prominent U wave, depressed St segment)

 Atony of smooth muscle

• intestinal distention

• constipation

• paralytic ileus

• urinary retention

 Confusion or disorientation

Hypokalemia

K+ < 3.5 mEq

Management

 Administer KCL slowly and accurately

 dilute properly with other IV fluids

 can cause pain and necrosis of veins

 Bring pt out of immediate danger & restore gradually

 Consider discontinuing diuretic therapy

 Consider chloride for metabolic alkalosis

Hypokalemia

Nursing Responsibilities

 Monitor intake and output carefully

 Infuse parenteral potassium supplement, as ordered; always dilute 1st, and monitor ECG during infusion

 Teach the patient to eat foods high in potassium, particularly if he or she is receiving steroid or diuretic therapy; such foods include: orange juice, bananas, cantaloupe, peaches, potatoes, dates, apricots

Calcium

8.8 - 10 mg/dL

Major functions:

 Transmission of nerve impulses

 Cardiac muscle contractions

 Blood clotting factor

 Formation of teeth & bone

 Skeletal muscle contraction

 Requires:

 Vitamin D

 Parathyroid hormone (PTH)

 Calcitonin from thyroid gland

Hypocalcemia

Ca+ < 8.5 mg/dL

 Nutritional deficiency of calcium or Vitamin D

 Parathyroid deficiency d/t surgical removal

 Children & elderly d/t dietary deficiency

 Bone cancer: excess bone formation

 “Hungry Tumor” syndrome

 Treatment of prostrate cancer with estrogen depletes ECF calcium levels

 Blood transfusions

 preserve blood with citrate & this binds with calcium

 Renal failure

Hypocalcemia

Ca+ < 8.5 mg/dL

Manifestations:

 Chvostek’s sign

 Trousseau’s sign

 Dysrythmias:< threshold for depolarization in cardiac cells: ECG changes: prolonged QT interval

 Paresthesias: “pins & needles”

 Abdominal cramping & diarrhea

 Tetany, Seizures (severe hypocalcemia)

tetany: tingling in fingers and circumoral area; muscle spasms associated with pain in extremities and face

seizures: due to neuromuscular irritability

Hypocalcemia:

Nursing Responsibilities

 Institute and maintain seizure precautions

 Administer parenteral calcium, as ordered

 Do not add calcium to parenteral solutions containing bicarbonate or phosphorus; this will cause precipitate formation

 Administer calcium cautiously to a patient receiving digitalis; calcium potentiates the action of digitalis, increasing the risk of cardiac arrest

 Maintain a relaxed, quiet environment

Hypercalcemia

Ca+ > 10.5 mg/dL

Malignancies or hyperparathyroidism

 PTH secreting tumor (adenoma)

 Skeletal calcium secreted into bloodstream

 Metastatic breast cancer & multiple myeloma

 Prolonged immobility: lose Ca+ from bone into blood

 Osteoporosis: Ca+ is liberated into bloodstream

 Manifestations:

 lethargy/ weakness/fatigue/constipation

 pathogenic fractures  calcium loss from bone

Hypercalcemia:

Nursing Responsibilities

 Provide patient teaching on the causes and treatment of hypercalcemia, covering:

 The importance of early ambulation to reduce calcium loss from bones during hospitalization

 The need for daily weight-bearing activities

 Encourage adequate fluid intake and dietary fiber intake

 Administer parenteral saline solution, as prescribed, to dilute serum calcium and inhibit tubular reabsorption of calcium

Hypercalcemia:

Nursing Responsibilities

 Take injury prevention measures, such as:

 Keeping bed side rails up

 Keeping bed brakes locked

 Respositioning often

 Securing all invasive lines

 Treat the underlying cause, as ordered; therapies may include:

 Calcitonin for hyperparathyroidism

 Mithramycin and corticosteroids for malignancies

Phosphate (PO4 -)

3.0 - 4.5mg/dL or 1.8 - 2.6 mEq/L

 Stored with Ca+ in bones & teeth

 PO-4 & Ca+ are equilibrated

• > Ca+ = < PO-4

• excreted by kidneys

 Hypophosphatemia: < 2.7 mg/dL

 clinical manifestations

• confusion, weakness, seizures, numbness, coma

 Hyperphosphatemia: > 4.5 mg/dL

 common in renal failure

Hypophosphatemia:

Nursing Responsibilities

 Prevent hypophosphatemia, and ensure early detection by identifying high risk patients

 Assist in the treatment objective of returning the serum phosphorus level to normal range

 Assess for signs of hypercalcemia, which occurs in the presence of hypophosphatemia

 Increase dietary intake of phosphorus

 Administer parenteral phosphorus as ordered if the depletion is severe

Hyperphosphatemia:

Nursing Responsibilities

 Prevent hyperphosphatemia, and ensure early detection by identifying high risk patients

 Assist in the treatment objective of reducing serum phosphorus levels to within normal range

 Administer calcium supplements along with phosphate binders as ordered

 Prepare the patient for hemodialysis, which may remove excessive phosphorus

 Instruct the patient to avoid foods/meds containing phosphorus

Magnesium (Mg+)

1.5 - 2.5 mEq/L

 Second most abundant ICF cation

 essential for neuromuscular function

 changes in serum Mg+ levels effect other electrolytes

 Hypermagnesemia: > 2.5mEq/L

 muscle weakness, bradycardia, hypotension, diaphoresis, hot flushed skin, lethargy, coma

 Hypomagnesemia:< 1.5mEq/L

 increased neuromuscular irritability

• Muscle spasms, tetany, seizures, (+) Chvostek’s and Trosseau’s signs

Hypomagnesemia:

Nursing Responsibilities

 Teach the patient dietary sources: nuts, whole grains, cornmeal, spinach, bananas, and oranges; encourage increased intake of these foods

 Administer parenteral magnesium replacement therapy as prescribed

 Monitor for signs of magnesium toxicity

 Institute and maintain seizure precautions

 Monitor ECG and pulse for abnormalities: flattened T wave, prominent U wave, depressed ST segment

Hypermagnesemia:

Nursing Responsibilities

 Teach the patient about the adverse effects associated with overuse of magnesium-containing antacids

 Monitor cardiovascular status closely

 Institute safety precautions, such as:

 Keeping bed side rails up

 Keeping bed brakes locked

 Repositioning often

References

 Braxmeyer, D. L. & Keyes, J. L. (1996). The pathophysiology of potassium balance. Critical Care Nurse, 16(5), 59-71.

 Hansen, M. (1998). Pathophysiology: Foundations of disease and clinical intervention. Philadelphia: Saunders.

 Huether, S. E., & McCance, K. L. (2002). Pathophysiology. St. Louis: Mosby.