pH Flashcards
What effect does acidaemia have on the concentration of potassium in the blood?
Increased [H+] in blood —> H+ ions buffered by moving into cells in exchange for K+ —> increased [K+] in blood —> decreased K+ gradient in cells —> decreased resting membrane potential —> prolonged depolarisation —> cardiac arrhythmias —> cardiac arrest
+ decreased K+ excretion in distal nephron
What are the effects of acidaemia on proteins?
Protein denaturation
- –> affects glycolysis
- –> affects muscle contractility
- –> affects hepatic function
How is blood pH calculated?
pH = 6.1 + log10([HCO3-]/pCO2 x 0.23)
Where is most HCO3- made?
RBCs (via carbonic anhydrase)
Summarise the filtration of HCO3- in the kidney.
Filtered in glomerulus and recovered in the PCT
H2O & CO2 diffuse across tubular cell membrane
Form H+ and HCO3-
HCO3- transported into ECF via HCO3-/Na+ transporter (driven by Na+ gradient created by Na+/K+-ATPase)
H+ transported back into lumen of PCT via NHE (driven by Na+ gradient created by Na+/K+-ATPase)
Summarise how H+ is excreted in the kidneys.
PCT:
Glutamine converted into NH4+ and alpha-ketoglutarate
NH4+ converted into NH3 & H+
NH3 & H+ diffuse into lumen of kidney
NH3 & H+ converted back into NH4+ (excreted)
alpha-ketoglutarate converted into 2HCO3-
HCO3- transported into ECF via Na+/HCO3- transporter (driven by Na+ gradient, created by Na+/K+-ATPase)
DCT:
- Principal cell: Na+/K+-ATPase
- alpha-intercalated cell:
HCO3- transported into ECF via Na+/HCO3- transporter (driven by Na+ gradient, created by Na+/K+-ATPase)
H+ actively transported into kidney lumen
H+ combines with HPO42- to form H2PO4-
Summarise the lab findings in respiratory acidosis (compensated and uncompensated).
RESPIRATORY ACIDOSIS =
- high pCO2 (hypoventilation —> hypercapnia)
- normal [HCO3-]
- reduced pH (due to hypercapnia)
COMPENSATED RESPIRATORY ACIDOSIS =
- high pCO2
- high [HCO3-] —> increases pH
- normal pH
Summarise the lab findings in respiratory alkalosis (compensated and uncompensated).
RESPIRATORY ALKALOSIS =
- low pCO2 (hyperventilation —> hypocapnia)
- normal [HCO3-]
- high pH (due to hypocapnia)
COMPENSATED RESPIRATORY ALKALOSIS =
- low pCO2
- low [HCO3-] —> reduces pH
- normal pH
Summarise the lab findings in metabolic acidosis (compensated and uncompensated).
METABOLIC ACIDOSIS =
- normal pCO2
- low [HCO3-]
- low pH
COMPENSATED METABOLIC ACIDOSIS =
- low pCO2 (hyperventilation stimulated by peripheral chemoreceptors)
- low [HCO3-]
- normal pH (hypercapnia)
Summarise the lab findings in metabolic alkalosis (compensated and uncompensated).
METABOLIC ALKALOSIS =
- normal pCO2
- high [HCO3-]
- high pH
Cannot normally compensate metabolic alkalosis (cannot reduce ventilation as pO2 needs to be maintained)
How is the anion gap calculated? What causes an increased anion gap, and why may the anion gap be normal?
([Na+] + [K+]) - (Cl-] + [HCO3-])
Increased anion gap = HCO3- replaced by other anions e.g. lactate, ketones, urate
Normal anion gap = HCO3- replaced by Cl- (so gap does not increase)
Give some examples of conditions causing respiratory acidosis and what the acute management is.
Type 2 respiratory failure e.g. COPD, severe asthma, drug overdose, neuromuscular disease
- low pO2 & high pCO2 (alveoli cannot be properly ventilated)
- chronic conditions well compensated for by increase in [HCO3-] so pH is near normal
- acute conditions more dangerous (takes time to compensate for)
e.g. COPD = put on non-invasive ventilation (BIPAP)
Give some examples of conditions causing respiratory alkalosis and what the acute management is.
Hyperventilation
- acute (anxiety/panic attacks) = low pCO2 & high pH
- chronic (Type 1 resp. failure) = low pCO2 & high pH —> low [HCO3-] to compensate —> decreases pH
+ over-ventilation in hospital whilst anaesthetised
e.g. hyperventilation = put on O2 mask but don’t give O2 (regulate breathing)
Give some examples of conditions causing metabolic acidosis and what the acute management is.
Increased anion gap =
- diabetic ketoacidosis
- lactic acidosis (exercising to exhaustion, poor tissue perfusion e.g. cardiogenic shock following MI)
- uraemic acidosis (advanced renal failure —> reduced acid secretion & build up of phosphates, sulfate, & urea)
e.g. DKA = insulin + fluids + K+ (although metabolic acidosis cause hyperkalaemia, treatment by insulin reverses this, and osmotic diuresis causes K+ to be lost in urine)
Normal anion gap =
- renal tubular acidosis (Type 1 = drug interactions with transport mechanisms in tubules, Type 2 = inability to pump out H+ or problems with HCO3- reabsorption)
- severe persistent diarrhoea (loss of HCO3-)
- contrast nephropathy —> AKI
- non-renal causes of increased K+ reabsorption by the kidneys or movement of K+ out of cells —> hyperkalaemia
e.g. contrast nephropathy = dialysis
Give some examples of conditions causing metabolic alkalosis and what the acute management is.
HCO3- retained in place of Cl-
- severe prolonged vomiting or mechanical drainage of stomach (loss of H+ —> H+ does not buffer HCO3- —> increased [HCO3-])
- reduced H+ excretion in nephron —> increased K+ excretion AND movement of K+ into cells —> hypokalaemia
- K+ depletion or mineralocorticoid excess
- loop or thiazide diuretics
- antacid overdose
e.g. antacid overdose = discontinue NSAIDs
