Fluid Electrolyte and Acid Base Balances

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Fluid Electrolyte and Acid Base Balances Powered By Docstoc
					          Biology 221
     Anatomy & Physiology II

        TOPIC 11
Fluid & Electrolyte Balance

                Chapter 27
               pp. 1041-1066

    E. Lathrop-Davis / E. Gorski / S. Kabrhel
             Fluid Compartments
• Intracellular fluid (ICF) = fluid within the cell
• Extracellular fluid (ECF)
   – plasma - fluid matrix of blood
   – interstitial fluid (IF) - fluid matrix of tissues

          Fig. 27.1, p. 1041
        Composition of Body Fluids
• Water = universal solvent
• Solutes
  – nonelectrolytes = not ionized; with or without
    electrical charge
     ° polar (hydrophilic) compounds such as
       carbohydrates, proteins that dissolve in
       water; have charged areas; and
     ° lipids and other nonpolar (hydrophobic)
       solutes that do not (e.g., O2, CO2)
  – electrolytes = particles that ionize in water to
    form anions (- charge) and cations (+ charge)
• Inorganic salts (e.g., NaCl, NaHCO3, MgCl2, KCl,
  CaCO3) – do not form H+ or OH- when they
   – HCO3- = bicarbonate; CO3= = carbonate
   – NaHCO3  Na+ + HCO3-
   – CaCO3  Ca2+ + CO3=
• Acids – dissociate to form H+ and an anion 
  lower pH
   – Inorganic acids (e.g., HCl)
   – Organic acids (e.g., H2CO3, amino acids, lactic
     acid, fatty acids, ketone bodies)
• Bases – dissociate to form OH- and cation (e.g.,
  NaOH), or accept H+ (e.g, NH3)  raise pH
   – Inorganic bases - e.g., NaOH, NH3
      ° NaOH: NaOH  Na+ + OH-
      ° NH3: NH3 + H+  NH4+
   – Organic bases - e.g., nitrogen bases of DNA
     and RNA
               ECF versus ICF
• ECF: higher in Na+, Cl-, HCO3-
• ICF: higher in K+, HPO42-, Mg2+, protein

                       Fig. 27.2, p. 1043
                  Water Balance
• Sources:
   – ingested water (from food or liquids)
   – metabolic water (from aerobic respiration in
      ° glucose + 6 O2  6 CO2 + 6 H2O
• Losses:
   – urine (60%)*
   – sweat
   – lungs
   – feces
   – skin

       See also Fig. 27.3, p. 1044   Fig. 27.4, p. 1044
 Water Balance: Regulating Intake
Thirst response by hypothalamus
• Thirst stimulated by:
   – dry mouth (sensation carried to hypothalamus)
   – increased osmolality of ECF in hypothalamus
• Results in urge to drink liquids

            Fig. 27.5, p. 1045
Water Balance: Obligatory Output
Obligatory water loss – not controlled
• Loss through lungs – air humdified during
  inhalation (necessary for gas exchange); some
  water lost with exhalation
• Some always lost through feces -
   – diarrhea – irritation of GI tract decreases
     residence time  less reabsorption  greater
     loss through feces
• Loss across skin – not completely water tight
Water Balance: Regulating Output
• Sweat – controlled for body temperature
  regulation, not fluid balance
• Urine output – controlled for water balance,
  electrolyte balance, pH balance and blood
   Regulating Urine Output: ADH
Antidiuretic hormone
• Protein hormone secreted by posterior pituitary
  in response to:
   – impulses from hypothalamus, which responds
     to increased osmolality of ECF (resulting in
     increased osmolality of IF in hypothalamic
   – presence of aldosterone in plasma
• Increases water permeability of collecting ducts
• Water follows osmotic gradient back into plasma
   facultative water reabsorption

                                     Fig. 27.7, p. 1049
        Regulating Urine Output:
• Steroid hormone secreted by zona glomerulosa
  of adrenal cortex
• Increases Na+ reabsorption in DCTs and CDs
• Reabsorption of Na+ adds to osmotic gradient in
  IF  water follows by osmosis  obligatory
  water reabsorption

                                   Fig. 27.8, p. 1050
       Regulating Urine Output:
Enhance urinary output (decrease water
• alcohol – inhibits ADH secretion
• caffeine and most other drugs – inhibit Na+
        Disorders of Fluid Balance
• Dehydration – water loss exceeds water intake
  over a period of time; solute concentration gets
  too high
• Hypotonic Hydration – cells have too much
  water (concentrations of cellular solutes
  becomes too dilute) due to excessive water
  intake or renal insufficiency

                              Fig. 27.6, p. 1046
Disorders of Fluid Balance: Edema
See Topics 4 - 6
Accumulation of fluid in IF caused by:
• increased BP – which increases movement of
  fluid from the plasma into the IF
• decreased lymphatic drainage
• inflammation – caused by histamine and other
  chemicals resulting in vasodilation and increased
  capillary permeability
• decreased blood proteins (due to decreased liver
  function, protein malnutrition, loss of proteins at
  glomerulus) – resulting in lower blood osmotic
  pressure to draw fluid back into blood
           Electrolyte Balance
• Electrolytes = charged particles
   – dissociate to form cations (+ charge) and
     anions (- charge)
   – include salts, acids, bases
• Salts
   – ionic compounds that form cations and anions
     other than H+ and OH- (hydroxide)
   – sources: foods, fluids (e.g., sodas), small
     amounts from metabolism
       Electrolytes: Salt Losses
• perspiration in hot environment – hotter
  environment means more sweat  more salts
  lost with water
• normal loss with feces
   – GI upset increases loss
       ° diarrhea – shorter retention time 
         less reabsorption  greater loss of salts
         as well as water
       ° vomiting  loss of salts as well as water
• urine – point of control for most important
  Important Electrolytes: Na+ & K+
• Na+ (sodium): main cation, accounts for 90-95%
  of all solutes in ECF
   – most important electrolyte in creating
     significant osmotic pressure
   – essential to neural and muscular function
• K+ (potassium)
   – important to neuron and muscle function
     function due to its influence on membrane
     potential (repolarization, hyperpolarization)
   – also influences acid-base balance (to be
     discussed shortly)
      Important Electrolyte: Ca2+
• important to neuron and muscle function
   – maintaining correct Na+ permeability of
     neuronal membranes
   – exocytosis of neurotransmitter
   – muscle contraction (all types)
   – action potential in autorhythmic cardiac cells
• other functions of Ca2+
   – clotting factor IV
   – important constituent of bone
         Other Important Ions
• Mg2+ (magnesium)
   – enzyme cofactor for carbohydrate and
     protein metabolism
   – important component of bone
• Cl- (chloride): main anion; follows Na+
   Control of Selected Ions: Sodium
• steroid hormone secreted by zona glomerulosa of
  adrenal cortex
• secreted in response to
   – high K+, low Na+
   – angiotensin II (renin-angiotensin pathway)
   – ACTH from adenohypophysis
• increases active reabsorption of Na+ from DCT
  and CD (without aldosterone, little Na+ is
  reabsorbed from DCT or CD)

                                    Fig. 27.8 p. 1050
   Control of Selected Ions: Sodium
• released by neuro-hypophysis (synthesized in
  hypothalamus) in response to increased Na+
  detected by hypothalamus increases water
  reabsorption to decrease plasma osmolality
• affects concentration by not total amount of

                               Fig. 27.7, p. 1049
   Control of Selected Ions: Sodium
Atrial natriuretic peptide (ANP; a.k.a., atrial
  natriuretic factor)
• released in response to elevated BP
• blocks reabsorption of Na+ (by decreasing
  aldosterone release)
• blocks ADH secretion
• inhibits renin release by kidney

                                         Fig. 27.10, p. 1052
  Control of Selected Ions: Sodium
• Estrogens
   – steroids produced by ovaries and zona
     reticularis of adrenal cortex
   – enhance Na+ reabsorption
• Glucocorticoids
   – steroids produced by zona fasciculata of
     adrenal cortex
   – enhance Na+ reabsorption
     Control of Sodium: Disorders
• hyponatremia = decreased blood Na+
   – neurological dysfunction (brain swelling;
     mental confusion, irritability, convulsions,
     progresses to coma; muscular twitching)
   – systemic edema (less osmotic pressure in
• hypernatremia = increased blood Na+
   – thirst
   – CNS dehydration leading to confusion,
     lethargy, progressing to coma
   – increased neuromuscular irritability leading to
     twitching and convulsions
       Control of Selected Ions:
• Regulated at CDs in cortex of kidney – K+
  secretion tied to Na+ reabsorption
• Most important factor in regulation is K+
  concentration in plasma
   – increased K+ directly stimulates cells of CDs
   – excess of K+ causes K+ to move into CD cells 
     secretion into filtrate
• Aldosterone – stimulates active secretion of K+
   Control of Potassium: Disorders
• hypokalemia = decreased blood K+
   – cardiac arrhythmias
   – muscular weakness
   – alkalosis (due to action of kidney)
   – hypoventilation (to compensate for alkalosis)
   – mental confusion
• hyperkalemia = increased blood K+
   – nausea, vomiting, diarrhea
   – at slightly elevated levels causes tachycardia;
     at severely elevated levels causes
     bradycardia; cardiac arrhythmias, depression
     and arrest
   – skeletal muscle weakness and flaccid paralysis
 Control of Selected Ions: Calcium
Parathyroid hormone (PTH) – increases plasma Ca2+
• parathyroid glands secrete PTH in response to
  decreased plasma Ca2+
• PTH acts on
   – gut – stimulates uptake by epithelial cells
     (works by increasing Vita. D formation in
   – bones – stimulates osteoclasts, inhibits
   – kidney – acts on DCT to increase active
     reabsorption of Ca2+ (also inhibits PO42-
     reabsorption to maintain balance between Ca2+
     and PO42-)
 Control of Selected Ions: Calcium
Calcitonin from thyroid
• secreted by parafolliclar cells of thyroid in
  response to increased plasma Ca2+
• generally, thought to be only really important
  during youth when bones are being remodeled
• stimulates osteoblasts, inhibits osteoclasts in
• actions of calcitonin result in decreased plasma
    Control of Calcium: Disorders
• Hypocalcemia – decreased blood calcium
  – tingling in fingers, tremors, convulsions,
  – depressed cardiac function
  – “bleeder’s disease”
• Hypercalcemia – increased blood calcium
  – bone wasting
  – kidney stones
  – nausea, vomiting
  – cardiac arrhythmias and arrest
  – depressed respiration
  – coma
      Control of Selected Ions:
• Second most abundant intracellular cation
• Important cofactor of enzymes involved in
  protein and carbohydrate metabolism
• Important component of bone
• Reabsorption inhibited by PTH
  Control of Selected Ions: Anions
• Cl- is major anion
   – follows Na+ actively or passively in PCT, DCT
     and CD to balance charge
• Most others passively reabsorbed; involves
  membrane proteins for transport
   – hence, transport maxima exist for most anions
   – any concentration in excess of transport
     maximum is excreted in urine
             Acid-Base Balance
• pH – measure of H+ concentration in a liquid
   – pH of distilled water (i.e., neutral) = 7.0
• Normal values
   – arterial blood = average pH 7.4
   – venous blood and interstitial fluid = pH 7.3
   – intracellular fluid (ICF) = pH 7.0 (neutral, but
     more acidic than other compartments)
• Protein function depends on H+ concentration
            Acid-Base Balance
• Acids – dissociate to form H+ and an anion
   – addition of H+ lowers pH
   – metabolic sources of acids:
      ° anaerobic respiration (produces lactic acid)
      ° protein catabolism (produces amino acids
        and keto acids)
      ° fat metabolism (produces fatty acids and
        ketone bodies)
• Bases – dissociate to form OH- and a cation, or
  sequester H+ (e.g., NH3)
   – removal of H+ or addition of OH- raises pH
         Strength of Acids/Bases
• Refers to ability to ionize (i.e., dissociate to form
  H+ or OH-)
• Strong acids/bases –
   – dissociate readily and completely
   – are usually inorganic (e.g., HCl, KOH, NaOH,
   – lead to large changes in pH when added to
     unbuffered solutions

                                       Fig. 27.11, p. 1056
   Strength of Acids/Bases (con’t)
• Weak acids/bases –
  – do not completely ionize (i.e., some of the
    molecular form remains)
  – are usually organic (e.g., H2CO3, NaHCO3,
    amino acids, fatty acids)
  – only change pH slightly when added to
    unbuffered solutions

                                      Fig. 27.11, p. 1056
         Acid-Base Balance:
       Chemical Buffer Systems
• Act quickly
• Involve exchange of strong acid/base for weak
• Three major chemical buffer systems
   – Bicarbonate buffer system
   – Phosphate buffer system
   – Protein buffer system
   Chemical Buffers: Bicarbonate
• Most important chemical buffer present in
  ECF; also buffers ICF
   – HCl + NaHCO3 --> H2CO3 + NaCl
   – NaOH + H2CO3 --> NaHCO3 + H2O
• Carbonic acid (H2CO3) levels affected by
  carbon dioxide availability (ventilation)
• Bicarbonate (NaHCO3) levels regulated by
     Chemical Buffers: Phosphate
• very important in ICF and urine
• HCl + Na2HPO4  NaH2PO4 + NaCl
• NaOH + NaH2PO4  Na2HPO4 + H2O
       Chemical Buffers: Protein
• very important in ICF
• also important in plasma
• based on presence of acidic (donate H+) and
  basic (accept H+) side chains of amino acids
• reduced hemoglobin = hemoglobin without O2
   – reduced hemoglobin takes on H+ (decreases
     free H+ increases pH)
          Acid-Base Balance:
          Respiratory System
• Acts more slowly (minutes)
• Respiratory compensation changes in
  ventilation make up for metabolic pH changes
   – CO2 + H2O  H2CO3  H+ + HCO3-
   – decreased pH (higher H+) stimulates
     medulla to increase ventilation  increases
     loss of CO2  less carbonic acid  pH
     increases (less H+)
   – increase pH (lower H+) decreases
     stimulation of medulla decreased ventilation
      decreases loss of CO2  CO2
     accumulates  more carbonic acid
           Acid-Base Balance:
           Renal Compensation
• Makes up for changes due to respiratory
• Kidney excretes or conserves HCO3-, depending
  on needs of body to make up for changes in
  respiration that cause pH imbalances
   – if pH decreases, HCO3- is conserved
   – if pH increases, HCO3- is excreted
            Acid-Base Balance:
            Renal Compensation
• Kidney excretes H+
   – if pH decreases, H+ is excreted
   – if pH increases, H+ is conserved
• Only kidney rids body of metabolic acids other
  than H2CO3
• H+ competes with K+ for removal (hyperkalemia
  can lead to decreased pH)
          Acid-Base Disorders
• Changes in pH result from respiratory or
  metabolic causes
• Factors that would cause increased pH if
  uncompensated = alkalosis
• Factors that would cause decreased pH if
  uncompensated = acidosis
 Disorders of Acid-Base Balance:
• Any condition that may lead to alkalemia
  (increase in arterial pH above 7.45)
• Respiratory Alkalosis
   – caused by hyperventilation
   – excessive loss of CO2  less H2CO3
• Metabolic Alkalosis
   – loss of H+ through vomiting
   – constipation (retention of HCO3-)
   – K+ depletion (stimulates secretion of H+)
   – excess aldosterone secretion (reabsorption
     of Na+ tied to loss of H+)
          Effects of Alkalemia
• Increased cardiac irritability and arrhythmias
• Compensatory hypoventilation (if cause is
• Vascular changes
   – Vasodilation
   – Spasm of coronary arteries
   – Decreased cerebral blood flow
• Seizures
• Increased blood lactate (lactic acid)
• Hypokalemia and hypocalcemia
  Disorders of Acid-Base Balance:
• Any condition that may lead to physiological
  acidosis (decrease in arterial pH below 7.35)
• Respiratory Acidosis – retention of CO2
   – hypoventilation
   – impairment of lung function
   Disorders of Acid-Base Balance:
           Acidosis (con’t)
• Metabolic acidosis
  – loss of HCO3- in diarrhea (decreased
    reabsorption time)
  – renal disease (failure of kidney to excrete H+)
  – excess alcohol intake (ethanol  acetic acid)
  – high K+ in ECF (competes with H+ for excretion;
    either one is countertransported with Na+)
  – lactoacidosis – build-up of lactic acid after
    heavy exercise or prolonged hypoxia
  – ketoacidosis – generation of ketone bodies due
    to improper glucose metabolism (starvation or
    diabetes mellitus)
           Effects of Acidemia
• Increased pulmonary resistance leading to
  pulmonary edema
• Decreased cardiac function (bradycardia,
  ventricular fibrillation)
• Vascular changes (venoconstriction, arterial
• Hyperkalemia
• Insulin resistance
• Coma
       Respiratory Compensation
• For metabolic acid-base disorders
• Metabolic alkalosis results in compensatory
• Metabolic acidosis results in compensatory
            Renal Compensation
• For respiratory acid-base disorders
• Respiratory alkalosis results in compensatory
  excretion of HCO3- or retention of H+
• Respiratory acidosis results in compensatory
   – excretion of H+ or retention of HCO3-
   – excretion of H+ may result in hyperkalemia

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