T2 L6: Arterial blood gases KPa

Cards (33)

  • What does ABG testing show?
    acid-base balance
    ventilatory status
  • What is respiratory acidosis?
    build up / retention of CO2 (volatile acid)
  • What are 'fixed acids' ?
    products from the oxidation of dietary substrates
    have to be physically eliminated from body, typically via kidneys / liver
  • What is metabolic acidosis?
    accumulation of fixed acids
  • What are the most important buffers in our body?
    bicarbonate
    phosphate + blood proteins
  • How do we detect an abnormal accumulation of fixed acids?
    the anion gap
  • What is the equation for the anion gap?
    Na - (Cl + bicarbonate)
    normal AG with this equation = 12
  • What are the main causes of anion gap acidosis?
    GOLD MARK
    Glycols (ethylene and propylene)
    Oxoproline
    L-LACTATE
    D-lactase
    Methanol
    Aspirin
    RENAL FAILURE
    KETOACIDOSIS
  • What are the 2 categories of metabolic acidosis?
    1. Anion gap acidosis: build up of an acid
    2. Non-anion gap acidosis: loss of bicarbonate
  • What is Renal tubular acidosis (RTA)?
    non-anion gap metabolic acidosis
    result in urinary loss of bicarbonate and a hyperchloremic acidosis
    GI losses
    Can be caused by:
    • Acetazolamide
    • XS chloride administration (IV with NaCl)
  • How is the approach to ABG interpretation?
    1. Examine pH, PCO2 and HCO3: if abnormal;
    2. determine primary process: Acidaemia / alkalaemia?
    3. if metabolic acidosis present; calculate anion gap
    4. identify compensatory process
    5. determine if mixed acid-base disorder present
    6. determine cause
  • What is Acidaemia?
    a low blood pH (< 7.36) due to an acidosis
  • What is Alkalaemia?
    a high blood pH (> 7.44) due to an alkalosis
  • What is alkalosis?
    low of volatile acid or an increase in bicarbonate
  • What is the compensatory response for respiratory acidosis?
    compensatory metabolic alkalosis (ie retain HCO3-)
  • What is the compensatory response for respiratory alkalosis?
    Compensatory metabolic acidosis (ie eliminate HCO3-)
  • What is the compensatory response for metabolic acidosis?
    Compensatory respiratory alkalosis (ie eliminate more CO2 )
  • What is the compensatory response for metabolic alkalosis?
    Compensatory respiratory acidosis (ie retain more CO2)
  • Difference between respiratory and metabolic compensation?
    respiratory compensation occurs more quickly
    metabolic compensation can take days
  • What is a 'mixed disorder'?
    two or more primary acid-base disturbances
    eg anion gap acidosis + non-anion gap acidosis at the same time
    Clues that a mixed disorder exists:
    1. The anion gap should be similar in value to the reduction in bicarbonate
    2. An anion gap is present but the pH is alkalaemic
    3. Incomplete compensation for any primary process.
    Reminder, “complete (ie full) compensation” does not result in a normal pH, but it gets close
  • What are the common causes of metabolic acidosis?
    Anion gap: GOLDMARK
    Non-anion gap: renal tubular acidosis (RTA), GI loss
  • What are the common causes of metabolic alkalosis?
    vomiting; increased aldosterone
  • What are the common causes of respiratoy alkalosis?
    hyperventilation due to pain or anxiety
    pregnancy
  • What are the common causes of respiratoy acidosis?
    increased dead space (emphysema)
    weakness
    depression of respiratory centre
  • What is the respiratory centre?
    Pons and medulla
    Dorsal respiratory group: control quiet breathing, trigger inspiratory impulses
    Ventral respiratory group: trigger inspiratory and expiratory impulses during exercise or other times of active exhalation
  • How can inputs alter the outputs of respiratory centre?
    Inputs from various sources can modify or modulate this rhythm:
    • Emotional inputs from the cerebral cortex
    • Lung receptors (see slide 30)
    • Chemosensors (central and peripheral)
  • What are the mechano- and irritant receptors in the lungs?
    1. C-fiber nociceptors: chemical mediators eg bradykinin, nicotine, histamine
    2. Mechanically sensitive receptors: cough receptors
    3. Lung stretch receptors: (hindbrain) help terminate inspiration and initiate exhalation
  • What is the ventilatory response to increased PaCO2 detected by peripheral chemosensors?
    increase ventilation
  • What are the peripheral chemoreceptors?
    • carotid body (PaO2, PaCO2, pH)
    • aortic body (PaO2, PaCO2)
  • What is the effect of opioids in chemosensor sensitivity to PaCO2?
    blunt sensitivity
    most common cause of acute hypercarbic respiratory failure
  • What is the ventilatory response to PaO2 detected by chemosensors as opposed to PaCO2?
    body much more sensitive to hypoxaemia in setting of hypercarbia
    so body much less sensitive to changes in PaO2 than PaCO2
    due to dual role of CO2 as by-product of respiration and as an acid
    body highly engineered to keep blood pH constant
  • What results will a loss of rubust respiratory drive show on ABG testing?
    Respiratory centre becomes less sensitive to chronic elevations in PaCO2
    respiratory response becomes blunted
    Result in:
    1. Chronic respiratory acidosis
    2. Metabolic compensation
    3. Hypoxaemia due to hypoventilation
  • What is 'base excess'?
    dose of an acid that would be needed to return blood to normal pH under standard conditions
    another way to measure presence of metabolic disturbance
    0 in normal blood
    increased in: metabolic alkalosis
    decreased in: metabolic acidosis