Lecture 28 - Acid/Base Physiology 3

Question 1

Metabolic alkalosis?

Answer 1

requires an initiator, and impaired renal function (HCO3 excretion usually increases)

Question 2

initiation of metabolic alkalosis?

Answer 2

gain of alkali in ECF (exogenous e.g. IV, or endogenous e.g. ketoanion metabolism) or loss of H+ from ECF (diuretics, vomiting, pyloric stenosis)

Question 3

Chloride depletion:?

Answer 3

lack of Cl- increases HCO3 reabsorption because only balancing anions for NA and K reabsorption; diuretics promoting loss of NaCl is a risk in volume depletion and when salt intake is low

Question 4

K depletion?

Answer 4

hyperaldosteronism (pri: Conn’s, sec: Bartters), distal tubular Na reabsorption with K+ loss, also H+ loss promoting HCO3 reabsorption, indirect effect of Na+ reabsorption increasing negative cell voltage promoting H+ secretion, also direct effect of stimulating ATPase - as a result upregulated anion exchange action (Cl/HCO3)

Question 5

Severe acidosis but normal bicarb?

Answer 5

bicard rises as a compensatory measure for respiratory acidosis, after a while metabolic acidosis occurs from lactic acid build up (indicated by low PaO2)

Question 6

Applying anion gap?

Answer 6

good tool for indication of cause of metabolic acidosis, ion of non-volatile acid being Cl- means normal anion gap (8-16) indicating diarrhoea or renal function, abnormal ion gap indicates lactate or ketone acidosis

Question 7

Alveolar gas equation?

Answer 7

enables PACO2 to be estimated form PaCO2, uses PIO2 -(PACO2/R), normally very small gradient at around 100mmHg; R is respiratory exchange ratio, typically 0.8

Question 8

Alveolar arterial gradient?

Answer 8

PAO2 - PaO2, >12mmHg young or >25mmHg old indicates impaired oxygen diffusion @ lung

Question 9

Systematic analysis?

Answer 9

1: pH - high or low; 2: PCO2, HCO3 & BE - acid or alk, resp. or metabolic; 3: compensated, uncompensated, simple or mixed?; 4: Anion gap; 5: PO2