Kidney: Acid-Base bBlance Flashcards
What kind of relationship between pH and plasma concentration of CO2
Inversely proportional (one goes up the other goes down)
What kind of relationship between pH and HCO3-?
Directly proportional
Normal body pH (extracellular fluid)
7.35-7.45
What fluctuations of pH does death occur?
- <6.8 (acidosis)
- > 8.0 (alkalosis)
2 types of sources of acid generation:
- carbolic (volatile) acids (15,000mmol/day)
- non-carbolic (non-volatile) acids
(70mmol/day)
Sources of acid generation: carbolic acids:
- generated from metabolism of carbs and
fats - produced as CO2 and converted to H+ and
HCO3- - reconverted back to CO2 in lungs and
eliminated by the lungs through the loss of
CO2
Sources of acid generation: Non-carbolic acids:
- generated from metabolism of sulphur
containing amino acids (proteins) - buffered with HCO3- before eliminated by
the kidneys through loss of H+
2 types of mechanisms of dealing with acid (H+) load:
- buffering
- elimination
Dealing with acid (H+) load: buffering (seconds):
- bicarbonate in extracellular fluid
- HPO42- in intracellular fluid
- carbonate in bones
Dealing with acid (H+) load: elimination:
- increased respiratory drive to increase CO2
excretion - acute response
- increased hydrogen ion secretion by
kidneys = chronic sustained response
3 systems
Normal ranges:
- blood pH
- urine pH
- blood HCO3-
- blood pCO2
Blood pH = 7.35 to 7.45
Urine pH = 4.6 to 8
Blood [HCO3-] = 22 – 26 mmol/L
Blood pCO2 = partial pressure of CO2 = 4.7 – 6.0 kPa
(35 – 45 mmHg)
Renal excretion of acid load in the PCT
- all parts of the nephron can excrete acid
- main sites are PCT and intercalated cells of
cortical collecting ducts - limited H+ secretion
- **Na+/H+ exchanger rebasorbs Na+ and
excretes H+ - ammonium is secreted into tubular fluid by
re-absorbing Na+ - 80%-990% filtered bicarb is re-absorbed
into systemic circulation - pH of ultrafiltrate falls from 7.4 to 6.7 at
end of PCT
Renal excretion of acid load in cortical collecting ducts:
- HPO42- is most prevalent filtered buffer in
DCT - not lipid soluble
- DCT urinary pH <5.8
- intercalated alpha cell
- ammonium excretion both in PCT and
direct diffusion of lipid soluble ammonia
constitutes a major adaptive response to
acid load
Maintaining renal tubular cell pH:
- decrease in extracellular bicarb
- increases grad across basolateral
membrane - diffusion out of cell
- hence lowers tubular cellular pH
- bicarb constant re-absorption creates
gradient allowing H+ ions to be secreted
Causes of acid base disorders
if diabetes then may present with diabetic ketone acidosis
sepsis causes lactate production
renal failure
Case 1: A 28 year old diabetic lady is admitted with high blood sugars following a viral illness.
Arterial blood gas on admission:
PH 7.0 (7.35-7.45), PCO2 3.5 Kpa (4.7-6.0), Bicarbonate 18 mmol/L (22-26)
- metabolic acidosis with compensation
- ph= acidic
- CO2 = low = metabolic
- bicarb = low
pH acidic hence she is acidotic, CO2 low because hypoventilating, kidneys compensating
hence diabetic ketoacidosis
Metabolic acidosis with compensation mechanisms
Case 2: A 72 year old female is admitted with exacerbation of COPD.
Arterial blood gas on admission
PH 7.0 (7.35-7.45), PCO2 8.5 Kpa (4.7-6.0), Bicarbonate 32 mmol/L (22-26)
- pH = low = acidosis
- CO2 = high = respiratory
- Bicarb = high = compensation (kidnery re-
absorbing to combat acid)
respiratory acidosis with compensation
Respiratory acidosis with compensation
Case 3: A 28 year with profuse vomiting for 2 days following a kebab meal.
Arterial blood gas on admission
PH 7.90 (7.35-7.45), PCO2 6.5 Kpa (4.7-6.0), Bicarbonate 32 mmol/L (22-26)
- pH = high = alkalosis
- CO2 = high = not respiratory but
compensation - bicarb = high = metabolic
Metabolic alkalosis with compensation
Metabolic alkalosis with compensation
Case 4: A 18 year anxious medical student is admitted with palpitations and light headedness a day before their final examination. He was tachypnoeic on admission with respiratory rate of 28/min.
Arterial blood gas on admission
PH 7.90 (7.35-7.45), PCO2 3.2 Kpa (4.7-6.0), Bicarbonate 20 mmol/L (22-26)
- pH = high = alkalosis
- CO2 = low = alkali = respiratory
- Bicarb = low = less rebasorbed =
compensation
Respiratory alkalosis with compensation
What are the compensatory responses?
Disorder: Metabolic acidosis
Primary abnormality: rise in plasma acid conc
A) Hyperventilation
B) Reduced ventilation
C) Renal Hydrogen excretion
D) Buffering of acid in extracellular fluid,
cells and bones
A) more breathing, expel CO2, acid
C) remove H+
D) combat H+
What are the compensatory responses?
Disorder: Metabolic alkalosis
Primary abnormality: rise in plasma bicarb conc
A) Hyperventilation
B) Hypoventilation
C) Reduced renal Hydrogen excretion
D) Reduced renal bicarb re-absorption
B) we want acid so we want CO2 so we
hypoventilate
D) we dont want alkali so lower re-uptake of
bicarb
What are the compensatory responses?
Disorder: Respiratory acidosis
Primary abnormality: rise in CO2
A) increase renal H+ excretion
B) increase buffering CO2 within Hb
C) Loss of bicarb in urine
D) increased renal bicarb re-absorption
A) want to remove acid
B) want to combat acid
D) want more alkali re-uptake
What are the compensatory responses?
Disorder: Respiratory alkalosis
Primary abnormality: reduction of CO2
A) increased renal bicarb re-absorption
B) reduced renal H+ excretion
C) Reduced renal ammonium excretion
D) increased renal bicarb excretion
B) want acid
D) want to remove alkali
Metabolic acidosis is frequently associated with hyperkalaemia or hypokalaemia?
Hyperkalaemia (high K+)
Metabolic alkalosis is frequently associated with hyperkalaemia or hypokalaemia?
Hypokalaemia
Metabolic acidosis treatment
- IV sodium bicarb
- IV furosemide (esp if passing urine)
- dialysis
Metabolic alkalosis treatment:
- IV sodium or Iv potassium chloride
Respiratory acidosis treatment:
ventilation
Respiratory alkalosis treatment:
breathing into a paper bag (hyperventilating)
Respiratory alkalosis compensation
