acid-base disorders

Question 1

what is normal blood pH

Answer 1

7.35-7.45

Question 2

acidosis

Answer 2

Disorder tending to make blood more acid than normal

Question 3

alkalosis

Answer 3

Disorder tending to make blood more alkaline than normal

Question 4

acidemia

Answer 4

Low blood pH

Question 5

Alkalemia

Answer 5

high blood pH

Question 6

pH

Answer 6

negative log [H+]

Question 7

falling pH =

Answer 7

increasing acidity

Question 8

base

Answer 8

accepts H+ ion

Question 9

acid

Answer 9

donates H+ ions

Question 10

what is standard bicarbonate

Answer 10

• Measures of metabolic component of any acid-base disturbance
• Absolute bicarbonate is affected by both respiratory and metabolic components
• Standard bicarbonate is the bicarbonate concentration standardised to pCO2 5.3kPa and temp 37
• Bicarbonate and std bicarbonate are calculated not actually measured

Question 11

what is base excess

Answer 11

• Quantity of acid required to return pH to normal under standard conditions
• Standard base excess (quantity of acid required to return extracellular fluid (ECF) back to normal)

Question 12

what do we measure in a ABG

Answer 12

• pH
• pO2
• pCO2
• Std HCO3-
• Std Base excess
• May include other measures (eg lactate, Na+, K+)

Question 13

what are 2 approaches to interpreting acid-base status

Answer 13

Henderson (o pH = pKa + log([A-]/[HA]))

Stewart’s theory (Strong ion difference (SID) SID = Na+ + K+ + Mg2+ + Ca2+ – Cl- – other strong anions (eg lactate, ketoacids))

Question 14

metabolic acidosis

Answer 14

causes
• Dilutional
• Failure of H+ excretion: Renal failure, hypoaldosteronism, type 1 renal tubular acidosis
• Excess H+ load: Lactic acidosis, Ketoacidosis, ingestion of acids (eg salicylate, ethylene glycol
• HCO3- loss: Diarrhoea, type 2 renal tubular acidosis
Clinical features: Sighing respirations (Kussmaul’s resps), tachypnoea
Compensatory mechanism: Hyperventilation to increase CO2 excretion

Question 15

anion gap

Answer 15

• Difference between measured anions and cations
• Anion gap = [Na+] + [K+] – [Cl-] – [HCO3-]
• Normal 10-16
• Wide anion gap: Lactic acidosis, ketoacidosis, ingestion of acid, renal failure
• Narrow anion gap (ie high chloride): GI HCO3- loss, renal tubular acidosis

Question 16

metabolic alkalosis

Answer 16

Causes:
• Alkali ingestion
• Gastrointestinal acid loss: Vomiting
• Renal acid loss: Hyperaldosteronism, hypokalaemia
Compensatory mechanism: Hypoventilation (but limited by hypoxic drive), renal bicarbonate excretion

Question 17

respiratory acidosis

Answer 17

• CO2 retention, leading to increased carbonic acid dissociation
• Causes: Any cause of respiratory failure
• Compensatory mechanism: Increased renal H+ excretion and bicarbonate retention (but only if chronic)

Question 18

respiratory alkalosis

Answer 18

• CO2 depletion due to hyperventilation
• Causes: Type 1 respiratory failure, anxiety/panic
• Compensation: increased renal bicarbonate loss (if chronic)

Question 19

urinary phosphate buffer (proximal tubule)

Answer 19

• H+, generated from the dissociation of H2CO3 from within the tubular epithelial cells, combines with HPO4 2- to form H2PO4- which is then excreted in the urine
• Increase in HCO3- concentration of the plasma – alkalinises it

Question 20

ammonium urinary buffer

Answer 20

• Tubular cells take up glutamine from both the glomerular filtrate & peritubular plasma and metabolise it to form NH3 & HCO3-
• The NH3 then reacts with the H+ in the cell to form NH4+
• The NH4+ is then actively secreted via Na+/NH4+ countertransport into the lumen and excreted, while the HCO3- moves into the peritubular capillaries and thereby increases HCO3- levels (net gain of HCO3-) alkalising the blood plasma