Acid base
Kidney contributes acid base homeostasis by
reclamation of bicarbonate in proximal tubule
generation of new bicarbonate in the distal tubule to replenish body buffer stores
active secretion of hydrogen ion
Daily filtered load of bicarbonate is 4500 mEq
Proximal tubular absorption of bicarbonate is increased by
ECF volume contraction
increase in Pco2
hypokalemia
Acid anion is filtered in glomerulus as sodium salt
H+ ion is excreted in distal nephron
factors increasing H+ secretion in distal nephron
aldosterone
elevated Pco2
Bicarbonate equivalent to H+ secretion is generated and absorbed in distal nephron
Normal pH is 7.38-7.42
pH values compatible with life 6.8-7.8
Bicarbonate is in both ICF and ECF and participates in buffering capacity
Acid production
Endogenous production of acid
combustion of glucose and fatty acids
carbon dioxide (volatile acid) and water
Handled by ventilation
Cellular metabolism
non volatile acids
Blood brain barrier
Freely permeable to co2
responses occur instantaneously
lag in equilibrating with bicarbonate
early stages of metabolic acidosis 2-3 hour lag in respiratory response
hyperventilation may persist even after correction of metabolic acidosis
Anion gap
anion gap = Na- (CL+HCO3)
Anion gap is due unmeasured phosphates, sulphates and albumin
the normal value for this anion gap is 10-12 mEq/l
increase in anion gap indicates metabolic acidosis
Metabolic acidosis
Normal anion gap
abnormally high bicarbonate loss
Kidney fails to reabsorb
renal tubular acidosis
Kidney fails to regenerate
Diuretics
extra renal loss of bicarbonate
Diarrhea
ileal drainage
acidifying salts have been added
hyperalimentation
ammonium chloride
Increased anion gap
reduced excretion of inorganic acids
renal failure
retention of sulphates and phosphates
impaired net acid excretion (ATN)
impaired ammonia excretion (Chronic renal failure)
accumulation of organic acids
ketoacidosis
diabetic
starvation
alcoholic
lactic acidosis (impaired cellular respiration with anaerobic glycolysis)
shock
septicemia
profound hypoxemia
ingestion
salicilates
methanol
Treatment
Renal failure: Bicarbonate is not required unless plasma bicarb falls below 16 mEq/L
Distal tubular acidosis: 30-60 mEq of bicarbonate daily
GI losses: Bicarb when the pH falls below 7.1
Lactic acidosis: improve tissue perfusion
Diabetic ketoacidosis: Insulin, bicarb only when the pH falls to 7.0-7.1
Metabolic alkalosis
loss of hydrogen ions from the body
vomiting
gastric suction
net rate of renal bicarbonate generation is greater than normal
volume contraction
potassium depletion
increased delivery of sodium to distal tubule (Loop diuretics)
minerelocorticoid excess
Rapid correction of ventilation in a patient with chronic CO2 retention
In severe alkalosis
Cardiac arrhythmia
Hypoventilation
Single vs. Mixed metabolic disorders
Single acid base disturbance: the change in concentration of one anion is balanced by a reciprocal change in one other anion.
Mixed acid base disturbance: the anion patterns are more complex
Respiratory acidosis
impaired alveolar ventilation
acute respiratory acidosis (normal bicarbonate)
narcotic overdose
respiratory muscle paralysis
acute airway obstruction
Chronic respiratory acidosis (increased bicarbonate)
COPD
kyphoscoliosis
Obesity hypoventilation syndromes
Respiratory alkalosis
Acute hyperventilation (Light headedness, paresthesias, circumvoral numbness, tingling of extremities and tetany.)
acute salicylism
fever
sepsis
CHF
PE
Mechanical ventilation
anxiety (breath with a paper bag)
Chronic hyperventilation
high altitude
hepatic insufficiency
pregnancy