Respiration 4

• Normal blood pH


  ~7.4 ±0.05
• Acidosis

  Values < 7.35
• Alkalosis

  Values > 7.45
• Acid-base buffer system


  • Mixture of a weak acid and its conjugate base, in approximately equal amounts
  • Release or bind H+ and stabilize pH
  • Acts within seconds

  
• Carbonic acid-bicarbonate buffer system


  • Carbonic acid - weak acid
  • Bicarbonate anion - its conjugate base
  • Most important in the ECF
  • Respiratory and renal systems act on this buffer system

  
• Phosphate buffer system

  • Dihydrogen phosphate - weak acid
  • Monohydrogen phosphate anion - weak base
  • Most important in the ICF and renal tubules

  
• Protein buffer system


  • The exposed carboxyl group of AA can release H+ when conditions are basic
  • The exposed amine group of the AA accepts H+
  • Proteins (plasma proteins – albumin, haemoglobin) can act as acids or bases
  • Important in ECF and ICF
  • Interact with other buffer systems

  
• Haemoglobin (Hb)

  • Principal protein inside of RBCs and accounts for one-third of the mass of the cell
  • CO2 diffuses across RBC membrane carbonic acid
  • Bicarbonate ions diffuse into plasma in exchange for chloride ions (chloride shift)
  • Hydrogen ions liberated in the reaction are buffered by Hb, which is reduced by the dissociation of oxygen
  • The process is reversed in the pulmonary capillaries to re-form CO2, which then can diffuse into the air sacs to be exhaled into the atmosphere

  
• Acid-base indicator


  • Weak acid or weak base that exhibits a color change as the concentration of H+ or OH- ions changes in an aqueous solution
  • Used in titration to identify the endpoint of an acid-base reaction
  • Used to gauge pH values
• pH scale

  • Measures acid and alkaline levels
  • Increase in acidity causes pH levels to fall
  • Increase in alkalinity causes pH levels to rise
• Respiratory acidosis


  • Primary increase in arterial PCO2 (primary hypercapnia) due to a decrease in respiratory rate and/or volume (hypoventilation)
  • Acute or chronic (based on the degree of metabolic compensation)

  
• Acute respiratory acidosis


  • PaCO2 is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.35)
  • Occurs when an abrupt failure of ventilation occurs
• Chronic respiratory acidosis


  PaCO2 is elevated above the upper limit of the reference range, with a normal blood pH (7.35-7.45) or near-normal pH secondary due to renal compensation and an elevated serum bicarbonate (HCO3 − >30 mm Hg)

  
• Mechanisms of increased arterial PCO2


  • Presence of excess CO2 in the inspired gas
  • Decreased alveolar ventilation
  • Increased production of CO2 by the body

  
• Respiratory alkalosis


  • Primary decrease in arterial PCO2 (primary hypocapnia) due to an increase in respiratory rate and/or volume (hyperventilation)
  • Acute or chronic (based on the degree of metabolic compensation)

  
• Metabolic compensation in chronic respiratory alkalosis

  Efficient and can result in normal arterial pH

  
• Causes of respiratory alkalosis

  • CNS stimulation: Fever, pain, anxiety, trauma, meningitis
  • Pulmonary disorders: Asthma, pulmonary oedema, pulmonary fibrosis, pulmonary embolism, pneumothorax
  • Hypoxemia: High altitude, severe anaemia, hypotension, cardiogenic shock
  • Medications and hormones: Salicylate, nicotine, progesterone
  • Miscellaneous: Exercise, sepsis, liver failure, heat exposure, pregnancy, recovery from metabolic acidosis

  
• Respiratory compensation for metabolic acidosis


  • Stimulation of respiratory centre increased respiratory rate to expel CO2
  • Occurs within minutes

  
• Respiratory compensation for metabolic alkalosis

  • Increase the amount of CO2 in the blood by decreasing the respiratory rate to conserve CO2
  • There is a limit to the decrease in respiration, hence, the respiratory route is less efficient at compensating for metabolic alkalosis than for acidosis