2535 Lecture 4: Notes on Fluid, Electrolyte, Acid-Base Homeostasis

fluid balance distribution

• ICF

• ECF

• Interstitial fluid

• intravascular fluid

• intracellular = 3rd space

• Tonicity

• Osmolarity

• fluid sources (oral intake, IV (iso-hypo-hyper)

• fluid losses (urine, feces, insensible losses)

tonicity - fluid balance distribution

osmotic pressure of two solutions separated by a semipermeable membrane

• isotonic = equal solute concentrations, causes no fluid shifts

• hypotonic = lower solute concentrations, causing water to shift into the cell = SWELL

• hypertonic = higher solute concentrations, causing water to shift out of the cell = SHRINK

osmolarity - fluid balance distribution

Osmosis: movement of water across a semipermeable membrane

• Water moves from an area of higher water concentration to an area of lower concentration

• Movement depends on hydrostatic (push) and osmotic (pull) pressure

controlling fluid balance - distribution  

• thirst mechanism

• ADH

• aldosterone

• atrial natriuretic peptide 

thirst mechanism - controlling fluid balance - distribution  

Thirst mechanism triggered by decreased blood volume and increased osmolarity

ADH -controlling fluid balance - distribution  

promotes reabsorption of water in the kidneys

aldosterone - controlling fluid balance - distribution  

increases reabsorption of sodium and water in the kidneys

atrial natriuretic peptide - controlling fluid balance - distribution  

stimulates renal vasodilation and suppresses aldosterone, increasing urinary output

fluid excess

• third spacing

• edema

• hypervolemia/fluid volume excess

• water intoxication

third spacing - fluid excess

significant fluid increases in the transcellular compartment, which does not exchange easily among other ECFs

edema - fluid excess

• Excess fluid in the interstitial space

• Anasarca: generalized edema

hypervolemia/fluid volume excess - fluid excess

Excess fluid in the intravascular space

water intoxication - fluid excess

Excess fluid in the intracellular space

causes of fluid excess

• excessive sodium or water intake 

  • High-sodium diet

  • Psychogenic polydipsia

  • Hypertonic fluid administration

  • Free water o Enteral feedings

  • Inadequate sodium or water elimination

  • Hyperaldosteronism o Cushing’s syndrome

  • Syndrome of inappropriate antidiuretic hormone

  • Renal failure

  • Liver failure

  • Heart failure

manifestations of fluid excess

• peripheral edema

• periorbital edema

• anasarca

• cerebral edema

• dyspnea

• bounding pulse

• tachycardia

• jugular vein distension

• hypertension

• polyuria

• rapid weight gain

• crackles

• bulging fontanelles

dx of fluid excess and deficit

• history, physical examination

• daily weights

• measurement of intake and output

• blood chemistry

• urine analysis

• complete blood count

treatment of fluid excess

• wearing compression stockings

• administering diuretics

• restricting sodium and fluids

• maintaining high Fowler’s position

• hypertonic solutions

fluid deficit

• dehydration

• hypovolemia or fluid volume deficit

  • decrease fluid in the intravascular space

  • can occur independently without electrocyte defects 

• Decrease in fluid level leads to increase in level of blood solutes, cell shrinkage, and hypotension

causes of fluid deficit

• Inadequate fluid intake:

  • Poor oral intake

  • Inadequate IV fluid replacement

• Excessive fluid or sodium losses:

  • Gastrointestinal losses

  • Excessive diaphoresis

  • Prolonged hyperventilation

  • Hemorrhage

  • Nephrosis

  • Diabetes mellitus

  • Diabetes insipidus

  • Burns

  • Open wounds

  • Ascites

  • Effusions

  • Excessive use of diuretics

  • Osmotic diuresis

manifestations of fluid deficit

• thirst, altered level of consciousness

• hypotension

• tachycardia

• weak and thready pulse

• flat jugular veins

• dry mucous membranes

• decreased skin turgor

• oliguria

• weight loss

• sunken fontanelles

treatment of fluid deficit

identify and manage underlying cause along with fluid replacement

sodium

• Normal range: 135–145 mEq/L

• Most significant cation and prevalent electrolyte of extracellular fluid

• Controls serum osmolality and water balance

• Plays a role in acid–base balance

• Facilitates muscles and nerve impulses

• Main source is dietary intake

• Excreted through the kidneys and gastrointestinal tract

• Depolarization: increase in membrane potential or excitability of the cell membrane

• Repolarization: restoration of resting potential

hypernatremia

Sodium >145 mEq/L

• Serum osmolarity increases ECF, resulting in fluid shifts OUT of cells (shrink) to ECF (high solute)

causes - hypernatremia

• Excessive sodium (dietary sodium, hypertonic IV saline, Cushing’s syndrome, corticosteroid use)

• Deficient water (insufficient intake, third spacing, excessive output, prolonged hyperventilation, diuretic use, diabetes insipidus)

manifestations - hypernatremia

• increased temperature

• warm and flushed skin

• dry and sticky mucous membranes

• dysphagia

• increased thirst

• irritability

• agitation

• weakness

• headache

• seizures

• lethargy

• coma

• blood pressure changes

• tachycardia

• weak and thready pulse

• edema

• decreased urine output

dx - hypernatremia and hyponatremia

• history

• physical examination

• blood chemistry

• urine analysis

treatment - hypernatremia

• fluid replacement (oral or hypotonic saline solution)

• diuretics

hyponatremia

Sodium <135 mEq/L

• Serum osmolarity decreases, low solute ECF, leads to increase solute in cells = increase H2O in cells = SWELL

causes - hyponatremia

• Deficient sodium (diuretic use, gastrointestinal losses, diaphoresis, insufficient aldosterone, adrenal insufficiency, dietary sodium restrictions)

• Excessive water (hypotonic IV saline, hyperglycemia, water intake, renal failure, syndrome of inappropriate antidiuretic hormone, heart failure)

manifestations - hyponatremia

• anorexia

• gastrointestinal upset

• poor skin turgor

• dry mucous membranes

• blood pressure changes

• pulse changes

• edema

• headache

• lethargy

• confusion

• diminished deep tendon reflexes

• muscle weakness

• seizures

• coma

treatment - hyponatremia

• limit fluids

• increase dietary sodium 

chloride

• Normal range: 98–108 mEq/L

  • Mineral electrolyte and major extracellular anion

• Found in gastric secretions, pancreatic juices, bile, and cerebrospinal fluid

• Plays a role in acid–base balance

• Main source is dietary intake

• Excreted through the kidneys

hyperchloremia

Chloride >108 mEq/L

causes - hyperchloremia

• Increased chloride intake or exchange: hypernatremia, hypertonic intravenous

  solution, metabolic acidosis, and hyperkalemia

• Decreased chloride excretion: hyperparathyroidism, hyperaldosteronism, and renal failure

manifestations - hyperchloremia and hypochloremia

reflect underlying cause

dx - hyperchloremia and hypochloremia

• history

• physical examination

• blood chemistry

• urine analysis

• arterial blood gases measurement

treatment - hyperchloremia

• identify and manage underlying cause

• diuretics

• bicarbonate

hypochloremia

Chloride <98 mEq/L

causes - hypochloremia

• Decreased chloride intake or exchange: hyponatremia, administration of 5%

  dextrose in water intravenous solution, water intoxication, and hypokalemia

• Increased chloride excretion: diuretics, vomiting, metabolic alkalosis, and other

  gastrointestinal losses

treatment -hypochloremia

• identify and manage underlying cause

• sodium replacement (oral or intravenous)

• ammonium chloride

• saline irrigation of gastric tubes

potassium

• Normal range: 3.5–5 mEq/L.

• The primary intracellular cation

• Plays a role in electrical conduction, acid–base balance, and metabolism

• Main source is dietary intake

• Excreted through the kidneys and gastrointestinal tract

• Serum potassium cannot fluctuate much without causing serious issue.

hyperkalemia

Potassium >5 mEq/L

causes - hyperkalemia

• Deficient excretion: renal failure, Addison’s disease, certain medications, and

  Gordon’s syndrome

• Excessive intake: oral potassium supplements, salt substitutes, and rapid

  intravenous administration of diluted potassium

• Increased release from cells: acidosis, blood transfusions, and burns or any other cellular injuries

manifestations - hyperkalemia

• paresthesia

• muscle weakness

• flaccid paralysis

• bradycardia

• dysrhythmias

• EKG changes

• cardiac arrest

• respiratory depression

• abdominal cramping

• nausea

• diarrhea

dx - hyperkalemia and hypokalemia

• history

• physical examination

• blood chemistry

• 12-lead EKG

• arterial blood gas

treatment - hyperkalemia

• correcting acidosis (sodium bicarbonate)

• calcium gluconate for dysrhythmias

• decreased dietary intake

• increased excretion (dialysis, IV solutions, meds)

• insulin

hypokalemia

Potassium <3.5 mEq/L

causes - hypokalemia

• Excessive loss: vomiting, diarrhea, nasogastric suctioning, fistulas, laxatives,

  potassium-losing diuretics, Cushing’s syndrome, and corticosteroids

• Deficient intake: malnutrition, extreme dieting, and alcoholism

• Increased shift into the cell: alkalosis and insulin excess

manifestations - hypokalemia

• muscle weakness

• paresthesia

• hyporeflexia

• leg cramps

• weak and irregular pulse

• hypotension

• dysrhythmias

• electrocardiogram changes

• decreased bowel sounds

• abdominal distension

• constipation

• ileus

• cardiac arrest

treatment - hypokalemia

identify and manage underlying cause along with potassium replacement (oral or intravenous)

calcium

• Normal range: 4–5 mEq/L

  • Mostly found in the bone and teeth

  • Plays a role in blood clotting, hormone secretion, receptor functions, nerve

    transmission, and muscular contraction o Has inverse relationship with phosphorus

  • Has synergistic relationship with magnesium

  • Main source is dietary intake (vitamin D aids absorption)

    • Absorbed through the gastrointestinal tract (small intestine)

    • Excreted in urine and stool

• regulated with vitamin K, parathyroid hormone, and calcitonin

hypercalcemia

Calcium >5 mEq/L

causes - hypercalcemia

• Increased intake or release: calcium antacids, calcium supplements, cancer,

  immobilization, corticosteroids, vitamin D deficiency, and hypophosphatemia

• Deficit excretion: renal failure, thiazide diuretics, and hyperparathyroidism

manifestations - hypercalcemia

• dysrhythmias

• EKG changes

• personality changes

• confusion

• decreased memory

• headache

• lethargy

• stupor

• coma

• muscle weakness

• decreased deep tendon reflexes

• anorexia

• nausea

• vomiting

• constipation

• abdominal pain

• pancreatitis

• renal calculi

• polyuria

• dehydration

dx - hypercalcemia and hypocalcemia

• history

• physical examination

• blood chemistry

• 12-lead EKG

treatment - hypercalcemia

• Identify and manage underlying cause

• Manage symptoms

• Phosphate

• Increase mobility

• Calcitonin

• Intravenous fluids

• Diuretics

hypocalcemia

Calcium <4 mEq/L

causes - hypocalcemia

• Excessive losses: hypoparathyroidism, renal failure, hyperphosphatemia, alkalosis, pancreatitis, laxatives, diarrhea, and other medications

• Deficient intake: decreased dietary intake, alcoholism, absorption disorders, and hypoalbuminemia

manifestations - hypocalcemia

• dysrhythmias, electrocardiogram changes, increased bleeding tendencies, anxiety, confusion, depression, irritability, fatigue, lethargy, paresthesia, increased deep tendon reflexes, tremors, muscle spasms, seizures, laryngeal spasms, increased bowel sounds, abdominal cramping, and positive Trousseau’s and Chvostek’s signs

• Trousseau sign: occlusion of arterial blood flow elicits carpal spasm

• Chvostek sign: tapping patient’s facial nerve prompts brief facial spasm

treatment - hypocalcemia

• Identify and manage underlying cause

• Calcium replacement (oral or intravenous)

• Vitamin D

• Decrease phosphorus (b/c inverse) 

phosphorus

• Normal range: 2.5–4.5 mg/dL

• Mostly found in the bones; small amounts are in the bloodstream

• Plays a role in bone and tooth mineralization, cellular metabolism, acid–base balance, and cell membrane formation o Main source is dietary intake

• Excreted through the kidneys

hyperphosphatemia

Phosphorus >4.5 mg/dL

causes - hyperphosphatemia

• Deficient excretion: renal failure, hypoparathyroidism, adrenal insufficiency, hypothyroidism, and laxatives

• Excessive intake or cellular exchange: cellular damage, hypocalcemia, and acidosis

manifestations - hyperphosphatemia

rarely seen alone

dx - hyperphosphatemia and hypophosphatemia

• history

• physical examination

• blood chemistry p

treatment - hyperphosphatemia

• Identify and manage underlying cause

• Aluminum hydroxide or aluminum carbonate

• Treat hypocalcemia

hypophosphatemia

Phosphorus <2.5 mg/dL

causes - hypophosphatemia

• Excessive excretion or cellular exchange: renal failure, hyperparathyroidism, and alkalosis

• Deficient intake: malabsorption, vitamin D deficiency, magnesium and aluminum antacids, alcoholism, and decreased dietary intake

manifestations - hypophosphatemia

similar to hypercalcemia 

treatment - hypophosphatemia

• Identify and manage the underlying cause

• Phosphorus replacement (oral or intravenous)

magnesium

• Normal range: 1.8–2.5 mEq/L

• An intracellular cation

• Mostly stored in the bone and muscle

• Plays a role in muscle and nerve function, cardiac rhythm, immune function, bone strength, blood glucose management, blood pressure, energy metabolism, and protein synthesis

• Main source is dietary intake

• Excreted through the kidneys

hypermagnesemia 

Magnesium >2.5 mEq/L

causes - hypermagnesemia

• renal failure

• excessive laxative

• antacid use

manifestations - hypermagnesemia

similar to hypercalcemia 

dx - hypermagnesemia and hypomagnesemia

• history

• physical examination

• blood chemistry 

treatment - hypermagnesemia

• diuretics

• dialysis

• intravenous calcium

hypomagnesemia

Magnesium <1.8 mEq/L

causes - hypomagnesemia

• inadequate intake

• chronic alcoholism

• malnutrition

• pregnancy

• diarrhea

• diuretics

• stress

manifestations - hypomagnesemia

similar to hypocalcemia

treatment - hypomagnesemia

magnesium replacement (oral or intravenous)

acid-base balance

• Measured by pH

  • Normal serum pH: 7.35–7.45

• Body fluids, kidneys, and lungs help maintain balance

• Subtle changes can cause serious effects

hydrogen concentration - pH regulation

• hydrogen is an acid

• more H+, the lower the pH

acids by-products of metabolism - pH

• volatile acids

• volatile gases 

• nonvolatile acids 

3 systems work to maintain acid-base balance

• buffers

• respiratory system

• renal system 

buffers

• Chemicals that combine with an acid or base to change pH

• Immediate reaction to counteract pH variations until compensation is initiated

4 major buffer systems

• the bicarbonate–carbonic acid system

• phosphate system

• hemoglobin system

• protein system 

bicarbonate-carbonic acid system

• Most significant in the extracellular fluid

• Carbonic acid and bicarbonate are the key players

• Carbonic acid forms from carbon dioxide reacting with water

• Carbonic anhydrase causes carbonic acid to separate into hydrogen and bicarbonate

• Carbonic anhydrase in the lungs allows for carbon dioxide excretion and in the kidneys allows for hydrogen excretion

phosphate system

• Similar to the bicarbonate–carbonic acid system

• Phosphates are in high concentrations in the intracellular fluid

• Some phosphates act as weak acids, and some act as weak bases

• This system primarily works in the kidneys by accepting or donating hydrogen

hemoglobin system

• Primarily occurs in the capillaries

• Acidity and hypoxia cause hemoglobin to release the oxygen

• Hemoglobin then becomes a weaker acid, taking up extra hydrogen

• Binding with oxygen makes hemoglobin more prone to release hydrogen

• Hydrogen reacts with bicarbonate to form carbonic acid, which is converted to carbon dioxide and released into the alveoli.

protein system

• Most abundant buffering system

• Proteins can act as an acid or a base by binding to or releasing hydrogen

• Occurs in the intracellular and extracellular spaces

• Hydrogen and carbon dioxide diffuse across the cell membrane to bind with protein inside the cell

• Albumin and plasma are the primary buffers in the intravascular space

note - re. buffers

• Potassium and hydrogen move interchangeably into and out of the cell to balance pH

• With extracellular excess, hydrogen moves inside the cell for buffering; in exchange, potassium moves out

• Potassium imbalances can lead to pH imbalances

respiratory regulation

• Manages pH by altering carbon dioxide excretion

• Speeding up respirations will excrete more carbon dioxide, decreasing acidity

• Slowing down respirations will excrete less carbon dioxide, increasing acidity

• Uses chemoreceptors

• Responds quickly, but is short lived

renal regulation

• Alters the excretion or retention of hydrogen or bicarbonate

• More effective because it permanently removing hydrogen

• Responds the slowest, but lasts the longest

compensation

• The body never overcompensates

• The cause of the imbalance often determines the compensatory change

  • If the problem causing the pH imbalance originates in the lungs, the kidneys initiate efforts to correct it

  • If the problem causing the pH imbalance originates outside the lungs, the lungs initiate efforts to correct it

acid-base disorders

• metabolic acidosis 

• metabolic alkalosis 

• respiratory acidosis 

• respiratory alkalosis 

metabolic acidosis 

Results from a deficiency of bicarbonate or an excess of hydrogen

causes - metabolic acidosis 

• Bicarbonate deficit: intestinal and renal losses

• Acid excess: tissue hypoxia resulting in lactic acid accumulation, ketoacidosis, drugs, toxins, and renal retention

anion gap - metabolic acidosis 

• Identifies the anions that are not measured

• Conditions that cause excess acid will increase the anion gap; otherwise, the anion gap is normal

• Normally, the sum of cations should be approximately equal to the sum of anions in the extracellular fluid

• Sodium is the most plentiful cation in the extracellular fluid; bicarbonate and chloride are the most abundant anions

determining anion gap - metabolic acidosis

bicarbonate and chloride results are added together and

subtracted from the sodium (normal anion gap is 6–9 mEq/L)

manifestations - metabolic acidosis

• Appear as regulatory systems fail to maintain pH within normal range

• Include headache, malaise, weakness, fatigue, lethargy, coma, warm and flushed skin, nausea, vomiting, anorexia, hypotension, dysrhythmias, shock, Kussmaul’s respirations, and hyperkalemia