Acid-base abnormality Flashcards
Define partial pressure
Contribution of one individual gas
within a gas mixture (such as air) to the total pressure
When gas dissolves in liquid (e.g. blood), the amount dissolved depends on the partial pressure.
Difference between PO2 and PaO2
PO2 = partial pressure of O2
PaO2 = partial pressure of O2 in arterial blood
How is PaCO2 controlled
PaCO2 is controlled by ventilation (respiratory centre in brainstem adjusts breathing rate via accessory muscles) and the level of ventilation is adjusted to maintain PaCO2 within tight limits.
THEREFORE high PaCO2 is always a sign of poor alveolar ventilation
Hypoxic drive: practical example
Give 28% Venturi mask O2 to COPD patients in T2RF
SO2 and SaO2
SO2 = O2 saturation in (any) blood
SaO2 = O2 saturation in arterial blood
Pulse oxymetry
- less accurate with saturations below 75%
- unreliable when peripheral perfusion is poor
- No PaCO2, so not a replacement for ABG in ventilatory impairment
What determines oxygen concentration in blood
SaO2 and Hb (not PO2)
If SaO2 and Hb determine O2 concentration in blood, what is the role of PO2
driving force for O2 molecules to bind to Hb: as such, it regulates the So2
Look at oxyhaemeglobin curve
3 factors that determine PaO2
- Alveolar ventilation
- Ventilation/perfusion (V/Q)
- Concentration of oxygen in inspired air (FiO2)
Why is alveolar ventilation important
Both oxygenation and CO2 elimination depend on alveolar
ventilation: impaired ventilation causes PaO2 to fall and PaCO2 to
rise.
What is V/Q mismatch
Not all blood flowing through the lung meets well-ventilated alveoli and not all ventilated alveoli are perfused with blood
V/ Q mismatch allows poorly oxygenated blood to re-enter the
arterial circulation, thus lowering PaO2 and SaO2.
Useful rule re FiO2 and PaO2
difference between Fio2 and Pao2 (in kPa) should not normally be greater than 10
Define hypoxia
Cells not getting enough O2 (either due to hypoxaemia or ischaemia)
Define hypoxaemia
Not enough O2 in blood
Define impaired oxygenation
hypoxaemia resulting from reduced
transfer of O2 from lungs to the bloodstream.
Causes of T1RF (usually V/Q mismatch)
Pneumonia
Acute asthma
Pulmonary embolism
Acute respiratory distress syndrome
Pneumothorax
Fibrosing alveolitis
Pulmonary oedema
COPD
Causes of T2RF (usually inadequate alveolar ventilation)
COPD
Opiate/benzodiazepine toxicity
Exhaustion
Inhaled foreign body
Flail chest injury
Neuromuscular disorders
Kyphoscoliosis
Obstructive sleep apnoea
Compensatory mechanisms in respiratory vs metabolic
Respiratory takes hours
Metabolic takes days
Dominant symptom in metabolic acidosis
Hyperventilation (Kussmaul breathing - fast & deep breaths)
Metabolic acidosis with raised anion gap
Ingestion of an exogenous acid or increased production of an
endogenous acid (increased H+)
M/C: Lactic acidosis
Others:
Ketoacidosis
Renal failure (accumulation of sulphate, phosphate, urate)
Poisoning (aspirin, methanol, ethylene glycol)
Massive rhabdomyolysis
Metabolic acidosis without raised anion gap
Excessive HCO3 loss, either renal (e.g. renal tubular acidosis) or GI (Diarrhoea = HCO3 loss)
Kidneys retain Cl- when HCO3 is lost i.e. hyperchloraemic metabolic acidosis
Other examples:
Adrenal insufficiency
Ammonium chloride ingestion
Urinary diversion (e.g. ureterosigmoidostomy)
Drugs (e.g. acetazolamide)
Lactic acidosis
Low HCO3 and lactate>4
Anaerobic metabolism as a result of ischaemia or profound hypoxaemia/shock
DKA
- A high anion gap metabolic acidosis
- hyperglycaemia
- The presence of ketones (detectable in blood or urine)
Metabolic alkalosis
Sustained vomiting or diuretics
M/C: Loss of gastric secretion (vomiting, NG suction)
Potassium depletion (e.g. diuretics)
Others:
Cushing syndrome
Conn syndrome (primary hyperaldosteronism)
Chloride-rich diarrhoea (e.g. villous adenoma)
Excessive administration of sodium bicarbonate
Kidney response to
1. Loss of Cl-
2. Loss of Na+ and K+
3. Result
- Loss of Cl- –> increase in HCO3 reabsorption
- Loss of Na+ and K+ –> increase in Na+ and K+ reabsorption at the expense of H+
- Metabolic alkalosis
Why is respiratory acidosis almost always uncompensated
metabolic compensatory responses take days to develop, acute
respiratory acidosis is almost always uncompensated, leading rapidly to
profound and dangerous acidaemia