Acid Base balance

• Extracellular fluid pH----7.35-7.45

• Plasma HCO3- deviations result in metabolic
acidosis or alkalosis
• Arterial CO2 deviations result in respiratory
acidosis or alkalosis
• Secondary compensation occurs within 12
to 24hrs for met acidosis and hrs to 2-5 days
for respiratory disorder.
• Simple acid –base disorder e.g diarrhoea
resulting in met acidosis or vomiting
resulting in met alkalosis
• Mixed acid - base disorder e.g D&V
• Mixed disorder in same direction e.g. met
acidosis & respiratory acidosis-- High risk –
life threatening
• pH –negative logarithm of hydrogen ion
concentration
• H+ ion conc---35 –45 nmEq/l corresponding to pH
7.45-7.35
• Lungs –excrete acid as CO2 (H2CO3) and kidneys
excrete H+ as ammonium acids and other
titratable acids.
• Severe acidosis---H+ conc >63nmEq (pH <7.20)
• Severe alkalosis– H+ conc <28nmEq (pH>7.55)
• Severe acidosis---depresses myocardial
contractility, sensitizes heart to arrhythmias,
arteriolar dilatation & hypotension, pulm
oedema
• Severe alkalosis---tissue hypoxia , mental
confusion and obtundation, muscular
irritability, sensitizes to seizures and cardiac
arrhythmias
 Buffer systems
• Buffer—a substance that reduces the change in free H+
conc of a soln on addition of an acid or base
• Extracellular buffers—HCO3- , Se proteins-- 1st line
• Intracellular buffers---proteins, phosphates, Hb---slow
buffers
• HCO3- ----- (H2CO3) system handles most extracell
buffering
• Arterial plasma HCO3- conc –1mEq/l <venous total CO2
content
• Henderson-Hasselbalch equation-------------pH =
pK + log (HCO3- / H2CO3)
• Modified Henderson-Hasselbalch equation pH =
pK + log (HCO3- / 0.03 x pCO2)
• Henderson equation (Kassier – Bleich
modification with out log) H+ = 24 x (pCO2/
HCO3- )
• Change in the ratio of pCO2 to HCO3- predicts
change in pH
 Compensatory systems
• Pulmonary Mechanisms
• Start immediately----take 12-24 hrs before
reaching steady state
• Increase RR stimulated by increase CO2
result in decrease CO2 thereby increases pH
• See table 1 --handout
• Renal Mechanisms
• Proximal tubule re-absorbs almost all
filtered bicarb—85%
• Distal tubule re-absorbs 15%
• Generation of bicarb in distal tubule
resulting in net secretion of H+ through
phosphate and ammonium buffers
 Acid base disorders
• Metabolic Acidosis—pH < 7.35
• Anion Gap----difference in unmeasured
serum anions and unmeasured serum
cations
• Measured cations—Na (140)
• Measured anions—Cl and HCO3 (102+26)
• Anion gap-- 12 (8-16) mEq/l
 Met acidosis
• Normal anion gap met acidosis
• See table 5 –handout
• Renal tubular acidosis---3 types
• Distal RTA (type 1)
• Proximal RTA (type2)
• Mineralocorticoid deficiency (type4)
 RTA
• Proximal—reduced proximal tubular re-
absorption of HCO3----due to carbonic
anhydrase deficiency
• <60% re-absorbed –vs 85%expected
• > 40% presented to distal tubules whose
capacity is for 15%--- 25% lost in urine
• Urine pH >6
 RTA
• Se bicarb decreases till urine losses cease—(se
bicarb 15-18 mEq/l)—all reabsorbed by distal
tubules
• Urine pH <5.5 then
• Na re-absorption results in
• K+ loss----hypoK+ ,
• chloride reabsorption ----hyperchloraemia
• Aldosterone secretion ---worsen K+ loss
• Causes ----See handout
 RTA
• Distal RTA
• Results from deficiency of H+ ion secretion by
distal tubule--- decreased formation of carbonic
acid ---
• loss of bicarb ---5-15% of filtered load
• Urine pH not below 5.8 despite severe acidosis
• Hyperchloraemia and hypoK+ ---not as severe as
in proximal RTA
• hypercalciuria
• +/- Nephrocalcinosis
 RTA
• Type 4—mineralocorticoid deficiency
• Inadequate production of or reduced distal tubular
responsiveness to aldosterone
• No aldosterone mediated Na reabsorption ---Na
loss– hyperkalaemia results
• HyperK+ --suppress renal ammonia production
---reduced net H+ excretion
• HyperK hyper Cl-acidosis results
• Urine pH maybe <5.5
• Treatment
• Treat underlying condition
• Correct acidosis
• Correct HypoK+
• Increased anion gap—diabetic
ketoacidosis---overproduction and under-
utilisation of ketoacids
– Lactic acidosis
– Ingestion of toxins –salicylate poisoning
 Metabolic Alkalosis
• See handout Table 8
• Pyloric Stenosis