Water Balance and Osmolality

Homeostasis

• A proper balance of fluids and electrolytes is needed to maintain equilibrium in the internal body environment.
• The composition of body fluids must be kept within narrow limits
• It is important for nurses to anticipate potential fluid and electrolyte imbalances and intervene with appropriate action.

H20

• Water makes up 60% of body weight
• Water content varies with sex, body mass, and age.
• Lean body mass has a higher percentage of water than adipose tissue.
• Older adults have lower water content due to decreased mass.

Regulation of Water Balance

• Water balance is maintained by the balance of intake and excretion
• Body fluid deficits, or increased plasma osmolality, are sensed by hypothalamic osmoreceptors, stimulating thirst and ADH release.
• ADH stored in the pituitary acts on the distal and collecting tubules of the kidney to reabsorb water.
• ADH is suppressed when plasma osmolality is normalized.
• Under normal conditions the body loses 900 ml of water per day due to insensible water loss.
• The kidneys produce about 1.5L of urine every day.

Patients at Risk for Hyperosmolality

• Patients who cannot recognize the sensation of thirst are at a significant risk
• Other Patients at risk are those with:
  • TBI or neurological disorders
  • Alzheimer's
  • Elderly
  • Diabetes
  • Certain Antipsychotics
  • Altered kidney function
  • Hormonal imbalances
  • Addisons (SIADH)

Mechanisms of Water Balance in the Body

Hypothalamic and Pituitary Regulation

• Body fluid deficits or increases in plasma osmolality triggers thirst and ADH secretion
• ADH released by the hypothalamus and stored in the pituitary.
• ADH acts on tubules of the kidney to retain water.
• When plasma osmolality is restored, ADH is suppressed and urinary excretion restored.

Adrenal Cortical Regulation

• Aldosterone (mineralocorticoid) is potent for sodium retaining and potassium excreting.
• A decrease in renal perfusion or decrease in sodium in the distal portion of the renal tubule activates RAAS and releases aldosterone.
• Aldosterone increases sodium and water reabsorption in the renal distal tubules, which leads to plasma osmolality decreasing and fluid volume being restored.

Cardiac Regulation

• Atrial natriuretic factor (ANF): hormone released by cardiac atria in response to increased atrial pressure and high serum sodium levels.
• Primary Actions of ANF: Vasodilation and increased urinary excretion of sodium and water decreases blood volume.

Sodium

• Sodium is the main cation of the ECF
• Changes in sodium are associated with parallel changes in osmolality
• Sodium is important in nerve impulse generation and transmission, and the regulation of acid base balance.
• A typical daily intake of sodium far exceeds the body's daily requirements.
• Sodium leaves the body through sweat, urine, and feces.
• Water follows sodium.

Hypernatremia

• Serum sodium may become elevated because of water loss or sodium gain.
• Hypernatremia is not typically a problem for a person who can sense thirst and is able to swallow.
• It Often results from impaired LOC or inability to obtain fluids
• Can also be caused by a deficiency in the synthesis of ADH, its release from the pituitary, or a decrease in kidney responsiveness to ADH: profound diuresis, water deficit, and hypernatremia.

Hypernatremia: Symptoms

• Thirst
• Lethargy
• Agitation
• Seizures
• Dry swollen tongue
• Normal or Increased ECF volume
• Weight Gain
• Peripheral and pulmonary edema
• Increased BP

Hypernatremia: Management and Nursing Interventions

• Hypernatremia is caused by either water loss or sodium gain
• Goal is to treat the underlying cause of hypernatremia
• Water deficit: fluid replacement orally or by IV with isotonic fluids to reduce serum levels gradually and minimize risk of cerebral edema
• Sodium Excess: dilute sodium with IV fluids such as 5% dextrose in water to promote excretion of sodium by administering diuretics
• Oral sodium restriction
• Pay attention to fluid intake and losses

Hyponatremia

• May result from a loss of sodium containing fluids, water excess, or a combination of both.
• The body attempts to compensate by shifting fluid out of the ECF and into the cells, leading to cellular edema
• Common causes of hyponatremia are the use of hypotonic fluids after a major trauma or surgery, or the administration of fluids in patients with renal failure.

Hyponatremia: Symptoms

• Cellular Swelling occurs
• Leads to Nonspecific neurological systems i.e headache, irritability, difficulty concentrating
• Also Severe confusion, vomiting, seizures and coma

Hyponatremia: Management and Nursing Interventions

• Infusion of hypertonic saline can be a method of treatment
• The patients serum sodium levels and response to treatment must be closely Monitored.
• Rapidly increasing levels of sodium can cause osmotic demyelination syndrome with permanent damage to nerve cells in the brain.
• May require fluid restriction

Effective Ways to Monitor Sodium and Volume Imbalances

• Monitor Intake and output
• Cardiovascular changes
• Respiratory Changes
• Neurological Changes
• Daily Weights
• Skin Assessment and care

Potassium

• K + is a major ICF cation
• Potassium is critical for many cellular metabolic functions:
  • Transmission of nerve impulses
  • Maintenance of normal cardiac rhythms
  • Skeletal smooth muscle contraction
• Diet is the typical source of potassium: fruit, dried fruits, vegetables
• Kidneys is the primary route for potassium loss
• Plays a role in acid base balance
• Sodium and Potassium have inverse relationship

Factors that Cause Potassium to Shift

• ECF - ICF - Insulin - Alkalosis - B-drenergic stimulation (stress, coronary ischemia)
• ICF- ECF
  • Trauma
  • Acidosis
  • Exercise
  • Digoxin

Hyperkalemia

• May be caused by:
  • Massive intake of potassium
  • Impaired renal excretion
  • Shift from ICF to ECF
  • Massive burn or crush injury
  • Certain drugs – spironolactone, ACE inhibitors
• *Most common cause is renal failure.

Hyperkalemia: Symptoms

• Causes membrane depolarization, altering cell excitability, causing them to become weak and paralyzed.
• First signs include leg cramping
• ECG findings may have a tall peaked T wave, may include a Wide QRS and prolonged PR interval
• Heart Block, V-Fib may occur

Hyperkalemia: Management and Nursing Interventions

• Eliminate oral and parenteral potassium intake
• Increase diuretics, dialysis, kayexalate
• Force K+ from the ECF to the ICF.
  • Administer IV insulin
  • Administration of IV sodium bicarb in the correction of acidosis
• Increasing fluid intake may enhance renal elimination
• Patients with a mild increase may be fine to have dietary potassium decreased and increase use of fluids and diuretics; Moderate increase will require shift of potassium back into cells

Hypokalemia

• Can result from abnormal loss due to shift from the ECF to ICF or deficiency in dietary intake
• The Most common cause is patients with diuresis, when circulating blood volume is low
  • Causes sodium retention and loss of potassium in urine
  • Low serum Mg contributes to potassium depletion
  • Low plasma Mg stimulates renin release and increase in aldosterone, potassium excretion
• GI tract losses
• Administration of insulin

Hypokalemia: Symptoms

• Alters membrane potential causing excitability problems
• Flat T wave, presence of U wave can be found on ecg.
• Paralysis of respiratory muscles, cramping, rhabdomyolysis can occur
• With prolonged hypokalemia kidneys unable to concentrate urine and diuresis occurs, release of insulin is impaired

Hypokalemia: Management and Nursing Interventions

• Develop habitual practices to be cognizant of patients' potassium levels
• Check AM labs always
• Always check before oral K+ administration, diuretics, digoxin
• Be aware of a patient's nutritional status, oral intake, fluid intake
• Know a patients diagnosis and pathology and how electrolyte balance will be affected
• Understand how an IV solution may cause fluid shifts

Calcium

• Calcium acquired from ingested foods

• Calcium levels are balanced by PTH, calcitonin, and Vit D

  • PTH increases bone resorption
  • Calcitonin opposes PTH by decreasing GI absorption and increasing excretion
  • Vit D is necessary for absorption from Gl tract

• More than 99% of body's calcium is combined with phosphorous and concentrated in skeletal system

• Calcium and phosphorous have inverse relationship, as one increases other decreases

• Calcium plays an important role in blood clotting, transmission of nerve impulses, formation of teeth, bone, and muscle contraction

Hypercalcemia

• More than 90% of cases caused by hyperparathyroidism and malignancy
• Excess calcium blocks effect of sodium in skeletal muscle reducing the excitability of muscles and nerves.
• Symptoms of note: Impaired memory Confusion, disorientation Fatigue Constipation Cardiac dysrhythmias Renal calculi.

Treatment of Hypercalcemia

• Promote excretion of Calcium in urine with loop diuretic (e.g. Lasix)
• Hydration of patient with isotonic saline
• Administration of synthetic calcitonin
• Provide Careful monitoring to avoid sodium and fluid overload for patients with impaired renal function

Hypocalcemia

• Can be caused by any condition that decreases PTH
• Could be due to injury to thyroid glands in neck after surgery
• Could be Due to sudden alkalosis as causes calcium to bind to protein Low calcium levels allow sodium to move into cells, causing increased nerve excitability and sustained muscle contraction.

Common Tests for Hypocalcemia

• Chvostek Signs: Contraction of facial muscles due to a light tap on the facial nerve by the ear.
• Trousseau's Sign: Carpal spasms induced by inflating a blood pressure cuff on the arm

Treatment of Hypocalcemia

• Treat any underlying conditions
• For Mild imbalance: eat calcium rick foods, take Vit D supplements
• For Severe Imbalances you can use IV preparations of calcium
• Any patient who has undone thyroid surgery must be monitored closely for manifestations of hypocalcemia because of their proximity to parathyroid glands.

Phosphate Imbalances

• Phosphorous is the primary anion of ICF
• Is Essential to muscle function, RBCs, and bone, and tooth structure
• Plays an important role Involved in acid base buffering system
• For the maintenance of normal phosphate balance, renal function must be adequate

Hyperphosphatemia

• Is Caused by acute or chronic renal failure that inhibits kidneys from excreting phosphorous
• Chemotherapy, malignancies, excessive injection of milk all can cause hyperphosphatemia
• Manifestations include:
  • CNS dysfunction
  • Rhabdomyolysis
  • Cardia dysrhythmias
  • Muscle weakness
  • Calcium-phosphate deposits in soft tissue, joints.

Treatment of Hyperphosphatemia

• Ensure adequate hydration
• Restrict foods that contain phosphorous
• Perform Correction of hypocalcemia conditions.

Hypophosphatemia

• Is Commonly seen in patients who are malnourished or have malabsorption
• Those with Alcohol withdrawal
• patients who Use phosphate binding antacids
• Clinical manifestations: relate to the deficiency of ATP, such conditions include:
  • Hemolytic anemia, muscle weakness

Treatment of Hypophosphatemia

• Provide Supplementation of high phosphorous containing food (e.g. dairy)
• IV treatment of severely low levels of phosphate.
• To guide IV therapy perform Frequent serum level monitoring

Magnesium Imbalances

• Most abundant intracellular cation, important role in intracellular processes Cofactor for many enzymes Carbohydrate metabolism DNA and protein synthesis
• Manifestations often confused with calcium imbalance as magnesium closely related to potassium and calcium; all three cations should be assessed together

Hypermagnesemia

• Commonly associated with patients who have chronic renal failure or ingesting products containing magnesium (milk of magnesia)
  • Excessive magnesium inhibits acetylcholine release at myneural junction and calcium movement into cells, impairing nerve and muscle function
• Key Manifestations:
  • Hypotension
  • Facial flushing
  • Lethargy
  • Urinary retention
  • Nausea and vomiting.
• As serum magnesium levels increase, deep tendon reflexes are lost, followed by muscle paralysis, and coma

Treatment of Hypermagnesemia

• Avoid magnesium containing medications
• Limit diet intake of nuts, bananas, oranges, and peanut foods
• If renal function is adequate, maintain increased fluids and promote urinary excretion
• In patients with impaired renal function, dialysis may be necessary
• If hypermagnesemia is symptomatic, administering calcium gluconate by IV infusion opposes the effect of magnesium on cardiac muscle

Hypomagnesemia

• Occurs in patients with limited magnesium intake or increased GI or renal losses
  • Starvation, chronic alcoholism, uncontrolled diabetes
• Manifestations mirror hypocalcemia:
  • Neuromuscular manifestations
  • Muscle cramps, tremors
  • Hyperactive deep tendon reflexes
  • Chvostek's sign
  • Trousseau's sign
• Can lead to cardiac dysrhythmias

Treatment of Hypomagnesemia

• Oral supplements, or increasing nutritional intake can help resolve hypomagnesemia
• Administer IV or IM MgS04
• If you are Administering IV Magnesium ,too rapid an infusion can lead to hypotension and cardiac or respiratory arrest

IV Fluids

• Commonly used to treat many different fluid and electrolyte imbalances
• Many patients need maintenance IV fluid therapy for losses that have already occurred

Hypotonic Solutions

• Provide more water than electrolytes, thus diluting the ECF and causing movement of water from ECF to ICF
• Maintenance fluids are often hypotonic because normal daily losses are hypotonic
• Hypotonic Solutions may cause cellular swelling
  • Do not give to stroke/head trauma patients.

Examples of Hypotonic Solutions

• D5W
• 0.45% NaCl

Isotonic Solutions

• Administration of an isotonic solution expands only the ECF, no net loss or gain from the ICF
• An Isotonic solution is an ideal fluid replacement for ECF deficit

Examples of Isotonic Solutions

• D5W – sort of
• 0.9% NaCl
• Lactated Ringers

When to Avoid Isotonic Solutions

• With NaCl ensure to monitor for hypernatremia
• Lactated Ringers: monitor for hyperkalemia

Hypertonic Solutions

• Initially raises osmolality of ECF and expands it
• Can be useful in treatment of hyponatremia and hypovolemia
• May be used in cases when a patient has ICP to draw fluid out of brain tissue and reduce swelling (mannitol)

Examples of Hypertonic Solutions

• D10W
• 3.0% NaCl
• D5W in 0.45% NaCL
• D5W in 0.9% NaCl

When to Avoid Hypertonic Solutions

• Avoid in patients who are dehydrated
• Avoid in patients who as hypernatremic
• Avoid if a patient has HF or is at risk of fluid overload
• Avoid if a patient has renal impairment

Acid Base Imbalances

• PH Range is 7.34-7.45
• Patients with DM, COPD, and Kidney disease are at risk for acid base imbalances
• Due to the body's metabolic processes, acids are constantly produced
• The body has 3 mechanisms in which it regulates acid base balance: - The buffer system. - The respiratory system - The kidneys

The Buffer System

• Reacts immediately to increase in H+ concentration
• Reaches maximum effectiveness within a few hours
• Buffers act to chemically neutralize strong acids by shifting H+ in and out of cell
• Carbonic acid, phosphate, protein, and hemoglobin
• Buffers minimize effect of acids on blood PH until they can be excreted from the body
• When ECF levels of H+ are increased, H+ enters cell in exchange for potassium. -This is why Alkalosis can cause hyperkalemia

Respiratory System Regulation

• Lungs help maintain PH of body by excreting CO2 and water
• Amount of CO2 in blood directly relates to carbonic concentration and H+
• Increased respiration rate leads to less CO2 in blood, leads to less carbonic acid and fewer H+ molecules
• Decreased respiration rate leads to increased carbonic acid and more H+ in blood
• If a PH problem is due to a respiratory condition, the Respiratory system may be unable to meet the usual role in pH correction.

Renal System Regulation

• Normal conditions for kidneys include absorbing and filtering bicarb, generating more bicarb and eliminating excess of H+ to correct the disturbance.

• If kidneys are cause of PH disturbance, e.g. renal failure, lose ability to correct PH Kidneys use 3 mechanisms for acid elimination

• Secretion of H+ in renal tubule

• Combining H+ with ammonia to form ammonium

• Excretion of weak acids

Respiratory Acidosis

• Blood pH is <7.35 and PaCO2 >45mm hg, this indicates respiratory acidosis
• Common Causes include: - COPD, Hypoventilation - Barbiturate overdose - Severe pneumonia - Atelectasis, respiratory muscle weakness
• Symptoms Include Drowsiness, Disorientation, Dizziness, Headache, Confusion, Coma
• Decreased BP, Vfib related to hyperkalemia from compensation, warm flushed skin due to vasodilation are also symptoms

Respiratory Alkalosis

• High blood PH (>7.45), indicates respiratory alkalosis low paCO2 (<35 mm Hg)
• Increased CO2 excretion from lungs
• Hyperventilation may be Caused by: Hypoxia , PE, Anxiety , Fear , Pain , Exercise
• In some case it can Be caused by Sepsis, and Brain injury.
• Symptoms include: Lethargy Lightheadedness and confusion Tachycardia, dysrhythmias related to hypokalemia Nausea, vomiting, numbness, hyperreflexia, seizures,

Metabolic Acidosis

• Has Low blood PH (<7.35) and a low HCO3- (<21 mmol/L)
• Can be from a gain of a fixed acid or inability to excrete acid or loss of base
• The following can lead to metabolic acidosis include: Diabetic Ketoacidosis Lactic acidosis Starvation Renal failure. Shock
• Key Symptoms to observe in patients: Drowsiness Confusion Headache Coma Decreased BP Dysrhythmias elated to hyperkalemia Warm flushed skin Nausea, vomiting, diarrhea Deep rapid respirations

Metabolic Alkalosis

• Metabolic labs indicate high blood PH (>7.45) and HCO3- (>28mmol/L)
• A patient may have also had a Loss of strong acid or gain of base Following can all contribute to Metabolic Acidosis
• Severe vomiting
• Excessive gastric suctioning
• Diuretic therapy
• Electrolytic deficiencies especially related to Potassium

Explore factors affecting water content in older adults versus younger individuals. Understand ADH's role in regulating water balance and triggers for its release. Also, identify conditions predisposing to hyperosmolality and the impact of lean body mass on total body water.