Fluids and Electrolytes, Acids and Bases

Fluids and Electrolytes, Acids and Bases

Distribution of Body Fluids

• Total Body Water (TBW) constitutes approximately 60% of body weight in adults.
• Body fluids are distributed into:
  • Intracellular fluid
  • Extracellular fluid:
    • Interstitial fluid
    • Intravascular fluid
    • Transcellular fluids: synovial fluid, CSF, GI fluids, pleural fluids, peritoneal fluids, and urine

Distribution of Body Fluids in Pediatrics and Aging

• Pediatrics:
  • TBW is 75% to 80% of body weight, making them more susceptible to significant changes in body fluids.
  • Newborns are particularly vulnerable to dehydration.
• Aging:
  • Decreased percent of total body water.
  • Decreased free fat and decreased muscle mass.
  • Renal decline.
  • Diminished thirst perception.

Cells & Homeostasis

• Diffusion:
  • The movement of a solute from an area of higher concentration to an area of lower concentration until there is equal concentration.
• Osmosis:
  • The movement of water through a semipermeable membrane from a lower solute concentration to a higher solute concentration until there is equal concentration.

Water Movement Between Fluid Compartments

• Hydrostatic pressure:
  • Pushes water out of capillaries (filtration).
• Osmotic/oncotic pressure:
  • Pulls water into capillaries (reabsorption).

Edema

• Excessive accumulation of fluid within the interstitial spaces.
• Causes:
  • Increase in capillary hydrostatic pressure.
  • Decrease in plasma oncotic pressure.
  • Increase in capillary membrane permeability.
  • Lymphatic channel obstruction (lymphedema).

Edema - Types, Symptoms, and Treatment

• Types:
  • Localized or generalized.
  • Effusion: Fluid accumulation in body cavities.
  • Anasarca: Severe generalized edema.
  • Dependent: Accumulation in gravity-dependent areas.
  • Pitting: Indentation remains after pressure is applied.
• Symptoms:
  • Swelling and puffiness.
  • Increase in body weight.
  • Tight-fitting clothes or shoes.
  • Functional impairment.
  • Pain.
  • Impairment of arterial circulation.
• Treatment:

Basic Facts of Sodium, Chloride, & Water

• Integral relationship between Na^+ and water levels.
• Chloride levels are generally proportional to changes in Na^+.
• Sodium balance is regulated by aldosterone.
• Renin and angiotensin are enzymes that promote the secretion of aldosterone, thus regulating sodium and water balance.
• Natriuretic peptides decrease tubular reabsorption and promote urinary excretion of Na^+.
• Water balance is regulated by the sensation of thirst and by antidiuretic hormone (ADH).

Renin-Angiotensin-Aldosterone System (RAAS)

• Maintains sodium/water balance in the body.
• Reduced circulation causes low renal perfusion, which stimulates renin secretion by the kidneys.
• Renin initiates the RAAS, a compensatory mechanism used to replenish blood volume and raise blood pressure (BP).
• Renin converts angiotensinogen to angiotensin I.
• In the lungs, angiotensin-converting enzyme (ACE) changes angiotensin I into angiotensin II (a powerful vasoconstrictor).
• Angiotensin II causes more vasoconstriction and aldosterone production.
• Aldosterone leads to sodium and water reabsorption back into the circulation and excretion of potassium.
• This results in increased blood volume.

Sodium and Chloride Balance

• **Sodium (Na^+
  • Primary ECF cation.
  • Regulates osmotic forces, thus water balance.
• **Chloride (Cl^-
  • Primary ECF anion.
  • Provides electroneutrality.

Water Balance

• Primarily regulated by antidiuretic hormone (ADH).
• ADH is secreted when plasma osmolarity increases or blood volume decreases.
• Increased osmolarity stimulates osmoreceptors, resulting in thirst, leading to fluid consumption and increasing body water.
• Osmoreceptors signal the posterior pituitary gland to release ADH, which increases water reabsorption by the kidneys into the plasma.
• Volume-sensitive receptors and baroreceptors also play a role.

Conditions Affecting Water Gain or Loss

• Gain:
  • History of heart disease, renal failure, or increased sodium intake.
• Loss:
  • History of hemorrhage, burns, diabetes insipidus.
  • Excessive sweating, vomiting, diarrhea, laxatives, or diuretic abuse.

Assessment of Water Gain or Loss

• Daily weights.
• Record 24-hour intake and output (I&Os).
• Monitor vital signs.
• Assess skin turgor.
• Assess urine characteristics, amounts, and specific gravity.
• Monitor Labs: BUN, creatinine, serum osmolarity.
• Assess for jugular vein distention.

Solutions

• Isotonic:
  • Solute concentration is equal to that of cells, keeping it in the intravascular space.
  • Examples: 0.9% NaCl (normal saline), Lactated Ringers (LR).
• Hypotonic:
  • Has a lesser concentration of sodium than cells, causing fluid to shift out of the intravascular space.
  • Example: 0.45% NaCl (half normal saline).
• Hypertonic:
  • Has a greater concentration of sodium than cells, drawing fluid into the intravascular space.
  • Examples: mannitol, 3% NaCl.

Alterations in Sodium, Chloride, and Water Balance

• Osmolality:
  • Used to evaluate the body’s hydration status based on the concentration of fluid and particles in a solution.
• Isotonic fluid alterations:
  • Occur when total body water changes are accompanied by proportional changes in the concentration of electrolytes (no change in concentration).
  • Normal isotonic imbalance: Serum osmolality = 280 – 294 mOsm/kg.
  • Isotonic fluid loss—hypovolemia.
  • Isotonic fluid excess—hypervolemia.

Isotonic Alterations: Water Balance in the Body

• Isotonic Fluid Loss (dehydration):
  • Causes: Mild vomiting, mild diarrhea, mild sweating.
  • Findings: Weight loss, dryness of skin and mucous membranes, decreased skin turgor, decreased urine output, symptoms of hypovolemia (rapid heart rate, flattened neck veins, and normal or decreased blood pressure, shock).
• Isotonic Fluid Excess:
  • Causes: Excessive administration of intravenous fluids, hypersecretion of aldosterone, drugs such as cortisone.
  • Findings: Weight gain, decreased hematocrit, distended neck veins, increase in BP, edema.

Alterations in Sodium, Chloride, and Water Balance - Hypertonic

• Hypertonic alterations:
  • Increased osmolality (>294 mOsm/kg).
  • Most common causes: Hypernatremia, water deficit in ECF (dehydration), or both.
  • The ECF hypertonicity attracts water from the intracellular space, causing ICF dehydration.

Hypertonic States

• Hypernatremic volume depletion:
  • Causes: Water deprivation, loss of thirst, inability to swallow, diabetes insipidus, excessive urination, excessive sweating.
  • Findings: Weight loss, weak pulses, increased heart rate, postural hypotension, excessive urination.
• Hypernatremic volume excess (serum sodium levels > 147 mEq/L):
  • Causes: Excessive intake of sodium compared to water.
  • Findings: Weakness, agitation, firm subcutaneous tissue, increased thirst, edema, elevated BP.

Alterations in Sodium, Chloride, and Water Balance - Hypotonic

• Hypotonic alterations:
  • Decreased osmolality (<280 mOsm).
  • Most common causes: Hyponatremia (Na^+ deficit), water excess in ECF.
  • Can lead to intracellular overhydration and cellular edema.

Hypotonic States

• Hyponatremic volume depletion (serum sodium levels < 135 mEq/L):
  • Causes: Vomiting, diarrhea, certain diuretic drugs, insufficient aldosterone, adrenal insufficiency.
  • Findings: Decreased urine formation, anorexia, nausea, cramps, fatigue, muscle weakness, headache, confusion, seizures, decreased BP.
• Hypotonic volume expansion:
  • Causes: Water excess, compulsive water drinking, syndrome of inappropriate secretion of ADH (SIADH).
  • Findings: Confusion and convulsions, muscle weakness, nausea, muscle twitching, headache.

Electrolyte Imbalance Overview

• For proper cell functioning, serum electrolytes must be kept in a narrow range.
• Na^+ is the main extracellular electrolyte, whereas K^+ is the main intracellular electrolyte.
• Na^+/K^+ pump is constantly at work to retain K^+ in the intracellular compartment and move Na^+ to the extracellular compartment.
• Alterations in sodium, potassium, and calcium affect neurotransmission and muscular contraction.
• Action potentials along neurons are disrupted.
• Cardiac rhythm abnormalities may develop.
• Skeletal muscle function is compromised.

Sodium (Na^+

• Normal range: 135-145 mEq/L
• Concentration is maintained by renal tubular reabsorption within the kidney in response to neural and hormonal influences.
• Accounts for 90% of ECF cations.
• In conjunction with chloride and bicarbonate (2 major anions), Na^+ acts to regulate water balance by contributing to extracellular osmotic forces.
• Roles: Regulates fluid balance between ECF & ICF, nerve impulse conduction, acid-base balance, cellular biochemistry, and the transport of substances across the cellular membrane.

Hyponatremia

• Serum sodium level <135 mEq/L
• Related to sodium loss or water gain (heart failure, diuretic therapy, excess water intake
• Manifestations are related to impaired nerve conduction and neurologic changes (confusion, lethargy, headache, tremors, seizures, weakness).
• Confusion and behavioral changes are common effects in elderly
• Cerebral edema & Increased intracranial pressure
• Treatment: Restrict fluid, provide oral supplements or 3% saline IV
• May encourage to consume sodium rich foods: bacon, butter, canned foods, cheese, lunch meat, etc.

Types of Hyponatremia

• Isovolemic:
  • Loss of sodium with normal water.
• Hypovolemic:
  • Loss of body water with a greater loss of sodium.
• Hypervolemic:
  • Increased body sodium causes increased body water.
• Dilutional:
  • Intake of large amounts of free water which dilutes sodium.
• Hypochloremia often occurs with hyponatremia.

Hypernatremia

• Serum sodium >145 mEq/L
• Related to sodium gain or water loss from dehydration, not drinking enough fluid, fever, diaphoresis, vomiting, diarrhea, kidney dysfunction, and diuretics.
• Manifestations are related to:
  • Brain cell shrinkage and altered membrane potentials
  • Confusion, fatigue, restless, agitation, irritability, increased fluid retention, edema, extreme thirst, dry mouth and skin, muscle twitching, and seizures.
• Treatment
  • Slowly give isotonic or hypotonic IV (D5W or 0.45%NS) preventing cerebral edema (can lead to seizures, coma, and death)
  • Low Na diet – avoid bacon, lunch meat, cheese, canned soup, boxed macaroni and cheese, etc.

Types of Hypernatremia

• Isovolemic:
  • Deficit of free water and near-normal sodium.
• Hypovolemic:
  • Loss of sodium and greater loss of body water.
• Hypervolemic:
  • Increase of body water with a greater increase in sodium.
• Hyperchloremia often occurs with hypernatremia.

Chloride

• Normal Value: 97-105 mEq/L
• Hypochloremia
• Hyperchloremia >105 mEq/L
  • Accompanies hypernatremia
  • Causes: increased Na^+ intake, hypertonic fluids, < water intake, corticosteroids, and metabolic acidosis
  • S&S: similar to >Na^+
  • Tx: aimed at addressing underlying cause

Potassium

• Major intracellular electrolyte (98% located in cells)
• Intracellular concentration: 150 to 160 mEq/L
• Extracellular concentration: 3.5 to 5.0 mEq/L
• Concentration gradient is maintained by Na ^+/K^+ ATPase pump
• Regulates intracellular electrical neutrality in relation to sodium (Na^+) and Hydrogen (H^+
• Roles: Maintains normal cardiac rhythms, facilitates glycogen/glucose deposition, skeletal and smooth muscle contraction, synthesis of ATP, and neuronal signaling.

Alterations in Potassium Levels

• Changes in pH affect K^+ balance
  • Hydrogen ions accumulate in the ICF during states of acidosis; K^+ shifts out to maintain a balance of cations across the membrane; result is hyperkalemia
• Aldosterone, insulin, epinephrine, and alkalosis influence serum potassium levels (shift K^+ into cells)
• Kidney is most efficient regulator
• Potassium adaptation
  • Slow changes are tolerated better than acute

Hypokalemia

• Potassium level <3.5 mEq/L
• Causes: reduced intake of potassium, increased entry of potassium into cells, increased loss of potassium, loop diuretics such as furosemide (Lasix), treatment of diabetic ketoacidosis (DKA) with insulin
• Also result from vomiting, diarrhea, intestinal drainage tubes, laxative abuse, excessive burns
• Manifestations
  • Depends on severity and rate of depletion
  • Membrane hyperpolarization causes a decrease in neuromuscular excitability, skeletal muscle weakness, smooth muscle atony, cardiac dysrhythmias, glucose intolerance, impaired urinary concentrating ability
• Treatment: administration of IV or PO supplements, potassium-rich foods such as avocados, bananas, spinach, beans, orange juice

Hyperkalemia

• Potassium level >5.5 mEq/L
• Hyperkalemia is rare because of efficient renal excretion
• Caused by increased intake, shift of K^+ from ICF into ECF, decreased renal excretion, compromised renal function, insulin deficiency, cell trauma secondary to burns and crush injuries, metabolic acidosis, and adrenal insufficiency
• Medications: ACE inhibitors, ARBs, and aldosterone antagonists – decrease renal potassium secretion. Potassium-sparing diuretics such as spironolactone (Aldactone)
• Treatment: Kayexalate or insulin combined with glucose; dialysis; monitor cardiac rhythm

Hyperkalemia Manifestations

• Depend on severity
• Mild attacks
  • Increased neuromuscular irritability
  • Restlessness, intestinal cramping, and diarrhea
• Severe attacks
  • Decreases the resting membrane potential
  • Muscle weakness, decreased cardiac contractility and arrhythmias, loss of muscle tone, and paralysis

Calcium

• Normal value = 8.8 to 10.5 mg/dl
• 99% of calcium is located in the bone as hydroxyapatite
• Necessary for metabolic processes, the structure of bones and teeth, blood clotting, hormone secretion, cell receptor function, plasma membrane stability, transmission of nerve impulses, muscle contraction
• Parathyroid hormone, vitamin D_3, and calcitonin act together to control calcium absorption and excretion

Hypocalcemia

• Decreased calcium concentration (<8.5 mg/dL)
• Causes: Inadequate intestinal absorption, deposition of ionized calcium into bone or soft tissue, blood administration, decreases in PTH and vitamin D, inadequate nutritional sources
• Effects: Increased neuromuscular excitability
  • Paresthesia of lips and fingers
  • Muscle spasm/twitching (hands, feet, facial & laryngeal muscles)
  • Positive Chvostek’s and Trousseau signs
  • Severe cases show convulsions and tetany; arrhythmias, prolonged QT interval, cardiac arrest
• Treatment:
  • Acute symptomatic: administer calcium gluconate IV push
  • Chronic: oral calcium + vitamin D supplements

Hypercalcemia

• Increased calcium concentration (>10.5 mg/dL)
• Causes: Hyperparathyroidism, bone tumors, excess vitamin D, tumors that produce PTH
• Effects
  • Many nonspecific: fatigue, profound muscle weakness, lethargy, anorexia, nausea, constipation
  • Impaired renal function, kidney stones
  • Dysrhythmias, bradycardia, cardiac arrest
  • Diminished or absent deep tendon reflexes
• Treatment
  • IV fluids and diuretics

Phosphate

• Normal value = 2.5-4.7 mg/dl
• Like calcium, most phosphate is located in the bone
• Provides energy for muscle contraction (as ATP)
• Parathyroid hormone, vitamin D_3, and calcitonin act together to control phosphate absorption and excretion
• Obtained in foods like milk, egg, cheese, fish, nuts

Hypophosphatemia

• Decreased phosphate concentration (<2.5 mg/dL)
• Causes: Intestinal malabsorption related to vitamin D deficiency, use of magnesium and aluminum-containing antacids, alcohol abuse, respiratory alkalosis, hyperparathyroidism
• Effects: Conditions related to reduced oxygen transport by RBCs and disturbed energy metabolism, deranged nerve and muscle function
  • Severe cases show irritability, confusion, numbness, coma, convulsions
  • Respiratory failure, cardiomyopathies, bone resorption

Hyperphosphatemia

• Increased phosphate concentration (>4.7mg/dL)
• Causes: Renal failure, chemotherapy, long-term laxative or enema use, hypoparathyroidism
• Effects: Related to low serum Ca^+ levels (caused by higher phosphate levels) similar to results of hypocalcaemia
  • Prolonged cases show calcification of soft tissues in lungs, kidneys, and joints
• Treatment:
  • Calcium-based phosphate binders (Sevelamer)
  • Dialysis

Magnesium

• Normal value = 1.5 to 2.5 mEq/L
• Found in the intracellular fluid and 40% - 60% stored in bone
• Function: increases neuromuscular excitability, role in smooth muscle contraction and relaxation
• Absorbed in the intestines, eliminated in kidneys
• Obtained from leafy greens, vegetables, whole-grain, seeds, nuts
• Increase calcium or phosphorus decreases absorption of magnesium
• Decreased calcium or phosphorous increases absorption of magnesium

Hypomagnesemia

• Decreased magnesium concentration (<1.5mg/dL)
• Causes: Malnutrition, malabsorption syndromes, alcoholism, urinary losses (renal dysfunction, loop diuretics)
• Effects: Behavioral changes, irritability, confusion
  • Increased deep tendon reflexes, muscle cramps, ataxia, nystagmus, tetany, seizures
  • Tachycardia, hypertension
  • EKG changes
• Treatments: Replacing magnesium orally or intravenously

Hypermagnesemia

• Increased magnesium concentration (>3.0 mg/dL)
• Causes: Renal insufficiency or failure, excessive intake of magnesium-containing antacids, excessive replacement for low magnesium, adrenal insufficiency (Addison disease)
• Effects: Decreased or loss of deep tendon reflexes, muscle weakness
  • Nausea and vomiting
  • Hypotension; bradycardia; heart block; impaired breathing (skeletal muscle weakness)
• Treatment: IV calcium, diuretics, dialysis

Acid-Base Balance

• Acid-base balance is carefully regulated to maintain a normal pH via multiple mechanisms (mainly lungs and kidneys)
  • Small changes significantly alter biologic processes
  • Normal pH arterial blood 7.35 – 7.45
  • If the H^+ are high, the pH is low (acidic)
    • pH <7.40 = acidic
  • If the H^+ are low, the pH is high (alkaline)
    • pH > 7.40 = alkaline

pH

• Acids are formed as end products of protein, carbohydrate, and fat metabolism
• Acids are substances that donate H^+
• To maintain the body’s normal pH, the acids must be balanced by base substances
• Bases are substances that accept H^+
• The lungs and kidneys are the major organs involved in the regulation of acid-base balance

Maintenance of Normal pH

• Mechanisms to maintain normal pH
  • Physiologic (chemical) buffer systems
  • Respiratory acid-base control
  • Renal acid-base control

Buffer Systems

• Buffer systems help prevent large changes in pH by:
  • Donating H^+ when solution is too basic
  • Absorbing H^+ when solution is too acidic
• Buffer systems:
  • Protein buffering
    • Proteins have negative charges, so they can serve as buffers for H^+
  • Renal buffering
    • Phosphate buffer and ammonia buffer are active in renal tubules
  • Bicarbonate-carbonic acid buffering

Bicarbonate-Carbonic Acid Buffering

• CO2 + H2O
  ightharpoonup H2CO3
  ightharpoonup HCO_3^- + H^+
• Carbon dioxide combines with water forming carbonic acid
  • CO2 + H2O
    ightharpoonup H2CO3
• Carbonic acid dissociates to form one H^+ (acid) and one bicarbonate (HCO_3^-) (base)
  • H2CO3
    ightharpoonup HCO_3^- + H^+
• Reversible to help maintain pH
• Operates in the lung and the kidney
  • Lungs adjust the amount of carbon dioxide
  • Kidneys reabsorb or regenerate HCO_3^- and excrete H^+ in urine

Acid-Base Imbalances

• Changes in H^+ concentration lead to acid-base imbalances
  • Acidosis: Systemic increase in H^+ concentration or decrease in bicarbonate (base)
  • Alkalosis: Systemic decrease in H^+ concentration or increase in bicarbonate (base)

Acid-Base Imbalances - Compensation

• Renal compensation
  • Kidneys resorb HCO_3^- into the plasma and excrete H^+ into the urine
• Respiratory compensation
  • Lungs breath deeply and rapidly to rid the body of CO_2

Acid-Base Imbalances - Metabolic

• If the altered pH occurs secondary to biochemical processes within the body, it is said to be metabolic.
  • Metabolic acidosis:
    • Low pH, low HCO_3^-
    • Can occur with lactic acidosis secondary to poor perfusion or hypoxemia
    • Examples: renal failure, shock, diabetic ketoacidosis, ingestion of toxic substances
    • Early S&S are HA and lethargy, which can progress to confusion and coma in severe acidosis. Other symptoms include anorexia, N/V, D, abdominal pain
  • Metabolic alkalosis:
    • High pH, high HCO_3^-
    • Result of excessive loss of metabolic acids
    • Vomiting, prolonged nasogastric suctioning, hyperaldosteronism
    • S&S: weakness, muscle cramps, hyperactive reflexes, tetany, confusion, convulsion, and atrial tachycardia. Respirations may be shallow, with slow ventilation, as the lungs attempt to compensate by increasing CO_2 retention

Acid-Base Imbalances - Respiratory

• If the alteration in the pH is secondary to an issue with breathing, it is said to be respiratory.
  • Respiratory acidosis:
    • Low pH, high PaCO_2
    • Result of alveolar hypoventilation
    • Hypoventilation à hypercapnia
    • Common causes: depression of respiratory system, paralysis of respiratory muscles, disorders of the lungs and chest wall.
    • S&S: HA, blurred vision, breathlessness, restlessness, and apprehension; followed by disorientation, muscle twitching, tremors, convulsions, and coma.
  • Respiratory alkalosis:
    • High pH, low PaCO_2
    • Result of alveolar hyperventilation (deep, rapid respirations)
    • Hyperventilation à hypocapnia
    • Common causes: severe anxiety and hysteria, hypoxemia (heart failure, pneumonia, pulmonary emboli, or high altitudes), hypermetabolic states (fever, anemia, thyrotoxicosis), early salicylate intoxication, cirrhosis, and gram- sepsis
    • S&S: dizziness, confusion, paresthesia, convulsions, and coma

Arterial Blood Gas (ABG)

• Arterial blood gases are measured to determine which of the 4 alterations are present.
• Typically includes the following 4 parameters
  • The blood pH
  • PaCO_2 (carbon dioxide)
  • HCO_3^- (bicarbonate)
  • PaO_2 (oxygen)

ABG: Normal Ranges

• Normal Ranges
  • pH = acidosis or alkalosis 7.35 – 7.45
  • PaCO_2 = carbon dioxide (acid) 35 – 45 mmHg
  • HC0_3^- = bicarbonate (base) 22 – 26 mEq/L
  • Pa0_2 = oxygen 80 – 100 mmHg

ABG Analysis

1. Do we have acidosis or alkalosis? Hint: Look at the pH

2. Is this a respiratory or metabolic problem?

   • If PaCO_2 is abnormal, it’s a respiratory problem.
   • If HCO_3^- is abnormal, it’s a metabolic problem.

3. Is there compensation? (uncompensated, partially compensated, or

   • fully compensated) Hint: Look at the pH and the other system.

   	Acidosis	Normal	Alkalosis
   pH	<7.35	7.35 – 7.45	>7.45
   PaCO_2	>45 mmHg	35 – 45 mmHg	<35 mmHg
   HCO_3^-	<22 mEq/L	22 – 26 mEq/L	>26 mEq/L

ABG Analysis: ROME method

• Respiratory
  • Opposite
    • CO_2 ↓ pH ↑ = Respiratory Alkalosis
    • CO_2 ↑ pH ↓ = Respiratory Acidosis
• Metabolic
  • Equal
    • HCO_3^- ↓ pH ↓ = Metabolic Acidosis
    • HCO_3^- ↑ pH ↑ = Metabolic Alkalosis