Acid-Base Homeostasis (16) Flashcards
Acid production
Total CO2 25mol/day
Unmetabolised acids 50 mmol/day (urine, sulphuric acid, phosphoric acid)
Plasma [H+] 40nmol/L
Buffering systems
Hb, bicarbonate, phosphate, proteins, ammonia, organic acids
pH
[H+]
Normal pH
7.45-7.35
Normal [H+]
35-45 nmol/L
[H+]
low - alkolotic, high-acidotic
Henderson-Hasselbalch equation
H+ + HCO3- H2CO3 CO2 + H2O
pH = pK + log ([HCO3-]/[pCO2] x a)
[H+] homeostasis requires
Balance between H+ production and regeneration of HCO3-
Sites of acid-base metabolism
Lungs, kidney, GI tract, liver
Tissue gas exchange
CO2 non-polar, easily pass into RBC, if acidify RBC changes shape and releases O2 > lungs
RBC equation
H+Hb+O2 > HbO2 > H+ + HCO3 (CO2/Cl-)
When does haemoglobin dissociated curve shift right?
Right shift Increased 2,3 diPG H+ acidosis Temperature
Kidney
- Bicarbonate is lost (active Na+/H+ pump)
- Regeneration of bicarbonate in renal tubule
- Distal tubercle under aldosterone control - regulates salt and water (Na+ secreted, K+ absorbed)
GI
Stomach secretes [H+], pancreatic juice [HCO3-]
Liver
Dominant site of lactate metabolism, only site of urea synthesis
Severe liver failure
Metabolic alkalosis, NH4+ toxicity
NH4+ + oxo-glutamate X>X glutamine
NH4+ + CO2 X>X urea and H+
Compensatory mechanisms
Respiratory, renal bicarbonate regeneration, hepatic shift between urea synthesis and ammonia excretion
Normal [H+]
36-44 nmol/L
Normal Na+
132-144 mmol/L
Normal K+
3.5-5.5 mmol/L
Normal Cl-
98-108 mmol/L
Normal HCO3-
21-28 mmol/L
Normal urea
Normal creatine
Metabolic acidosis
Increased H+ formation, acid ingestion, reduced renal H+ excretion, loss of bicarbonate (High H+, low CO2, high O2)
Metabolic alkalosis
Generation of bicarbonate by gastric mucosa, renal generation of HCO3- in hypokalaemia, administration of bicarbonate
(Low H+, high CO2, low pO2)
Consequences of metabolic alkalosis
K+ > cells and urine
PO4 > cells
Respiratory suppression
Respiratory acidosis
CO2 retention due to - inadequate ventilation and perfusion, parenchymal lung disease
(High H+, High CO2, Low pO2)
Respiratory alkalosis
Increased CO2 excretion - hyperventilation
Low H+, Low pCO2, High pO2
Causes of increased H+ formation
Ketoacidosis, diabetic, alcoholic, lactic acidosis, poisoning, inherited organic acidoses
Diabetic keto-acidosis
Hyperglycaemia, osmotic diuresis > pre-renal uraemia, hyperketonaemia, increase FFA
(all lead to acidosis)
Lactic acidosis
Shock or metabolic and toxic causes
Normal lactic acid levels
0.9-1.7 mmol/L
Acidosis in an alcoholic
NAD+ depletion (thiamine), thiamine deficiency (PDH co-factor), enhanced glycolysis for ATP formation, leto-acids (B-HBD) secondary to counter-regulatory hormones, profuse vomiting
In alkalosis
Increased glycolysis, reduced O2 delivery due to shift in O2 dissociation curve, lactate induced vasoconstriction, impaired mitochondrial respiration
O2 debt in alkalosis due to
Further anaerobic lactate production, hyperventilation
reduced H+ excretion
Renal tubular acidosis, generalised renal failure
Renal failure
Reduced volume of nephrons, increased bicarbonate loss, reduced NH4+ excretion, NH4+ to liver for urea and H+ synthesis, only fraction of NH4+ derived from glutamine (normal approx 100%)