Acid-Base Balance Disorders

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Acid-Base Balance Disorders

• LECTURE FROM PATHOPHYSIOLOGY
• 2012/2013
• OLIVER RÁCZ EVA LOVÁSOVÁ
• INSTITUTE OF PATHOPHYSIOLOGY
• UPJŠ LF KOŠICE

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Introductory remarks

• Acidobasic balance (ABB) First of all ABB of
  extracellular space blood
• 7,4 40 nmol/l H (or 410-7 mol/l )
• (not H but H3O)
• CO2 production 20 mols/day (300 360 l)
• Strong (non-volatile) acid production 60 70
  mmols/day
• oxidation of SH groups (amino acids) sulfate
• hydrolysis of proteins, phospholipids phospate
• keto acids, lactic acid...

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Logarithms
H Exp mmol/l pH pH nmol/l
100 mmol/l -1 1 7,1 79
10 mmol/l -2 2 7,2 63
1 mmol/l -3 3 7,3 50
100 mmol/l -4 4 7,4 40
10 mmol/l -5 5 7,5 31
1 mmol/l -6 6 7,6 25
100 nmol/l -7 7 7,7 20
10 nmol/l -8 8 7,8 16
1 nmol/l -9 9 7,9 12
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Physiological a pathological values

• pH H nmol/l
• 7,36 - 7,44 44 - 36
• 7,10 94
• 6,80 - 7,70 158 - 20
• 4,50 - 8,00 32000 10
• 7,28 53
• 6,90 126
• 6,2 - 8,5 631 - 3
• 6,5 - 7,6 316 - 25
• 4,50 32 mmol/l
• 1,2 - 3,0 1000 - 63

• Blood
• Physical exercise
• Frontiers of life
• Urine
• Red cells
• Muscle cells
• Bile
• Duodenal juice
• Prostata cells
• Gastric juice

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ABBMeasurement
Not very long ago...
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Astrup

• Arterial or arterialised capillary blood
  (hyperemisation of finger or auricle)
• 0,1 ml into heparinised capillary tube without
  air, immediate measurement
• pH and pCO2 electrochemically
• pCO2 5,3 0,53 kPa 1,2 0,12 mmol/l
• Other calculated
• actual bicarbonates 24 2 mmol/l
• anion gap 9 17 mmol/l
• standard bicarbonates as actual
• base excess 0 2 mmol/l
• buffer base 49 3

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Buffers and regulatory systems

• Buffers only absorb the attacks of hydrogen ions
  and prevent sudden big fluctuations of pH.
• Closed systems
• hydrogencarbonate
• phosphate
• haemoglobin/protein
• bones (carbonate)
• Regulatory systems open, regulate the
  hydrogencarbonate system
• respiratory (provisional, delayed)
• excretory (definite)

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Henderson and Hasselblach

• pH pK log HCO3/CO2
• pK 6,1
• HCO3 24 mmol/l
• CO2 40 mmHg 5,3 kPa 1,2 mmol/l
• pH 6,1 log (24/1,2) 6,1 1,3
• pH 7,4

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Acute and chronic Not compensated, partial
compensated, corriged
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Henderson and Hasselblach 1metabolic acidosis
something is decreasing bicarbonate (24)

• HCO3 12 mmol/l CO2 1,2 mmol/l
• pH 6,1 log (12/1,2) 6,1 1,0
• pH 7,1
• COMPENSATION THROUGH HYPERVENTILATION (CO2 OUT)
• HCO3 12 mmol/l CO2 0,6 mmol/l
• pH 6,1 log (12/0,6) 6,1 1,3
• pH 7,4 is everything OK???

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Henderson and Hasselblach 2metabolic alkalosis
too much of bicaarbonate

• HCO3 36 mmol/l CO2 1,2 mmol/l
• pH 6,1 log (36/1,2) 6,1 1,5
• pH 7,6
• COMPENSATION THROUGH HYPOVENTILATION (CO2)
  RETENTION
• HCO3 36 mmol/l CO2 1,8 mmol/l
• pH 6,1 log (36/1,8) 6,1 1,3
• pH 7,4 is everything OK???

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Henderson and Hasselblach 3respiratory acidosis
asfyxia

• HCO3 24 mmol/l CO2 2,4 mmol/l
• pH 6,1 log (24/2,4) 6,1 1,0
• pH 7,1
• COMPENSATION THROUGH ACID EXCRETION
• HCO3 48 mmol/l CO2 2,4 mmol/l
• pH 6,1 log (48/2,4) 6,1 1,3
• pH 7,4 is everything OK???

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Henderson and Hasselblach 4respiratory alkalosis
histeria, mountain sickness

• HCO3 24 mmol/l CO2 0,8 mmol/l
• pH 6,1 log (24/0,8) 6,1 1,5
• pH 7,6
• COMPENSATION THROUGH ACID RETENTION
• HCO3 16 mmol/l CO2 0,8 mmol/l
• pH 6,1 log (16/0,8) 6,1 1,3
• pH 7,4 is everything OK???

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Acids bind and decrease bicarbonate Respiratory
insufficiency increases CO2 Increased
bicarbonate Decreased CO2
MAC RAC MAL RAL
20 HCO3
1 CO2
7,4
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RAC, MAC, RAL, MAL
7,2
CO2
7,3
7,4
7,5
7,6
HCO3
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Compensation
7,2
CO2
7,3
7,4
7,5
7,6
HCO3
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Compensated disorders
7,2
CO2
7,3
7,4
7,5
7,6
HCO3
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Respiratory compensation of MAC

• Exspiration of CO2 (Kussmaul) balances the
  decreased bicarbonate
• Delayed respiration reacts to pH in the brain
• Danger delay also during treatment
• HCO3 and pH restored through treatment
• Hyperventilation persists
• Respiratory alkalosis!

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Kidneys

• Synthesis of bicarbonate in renal tubular cells
• H20 CO2 H2CO3 H -HCO3
• Complete resorbtion of bicarbonate into blood
• Maximal excretion of H through exchange for
  Na, K and by protone pump
• In filtrate H ions associate with ammonia and
  primary phosphate
• H NH3 NH4 H HPO42- H2PO4-

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Metabolic acidosispH lt 7,35 HCO3 lt 22 mmol/l

• Increased production of endogenous acids
  diabetic ketoacidosis, lactic acidosis
• Exogenous acids or compounds metabolised to acids
  ethylene glycol, methanol, salicylate
• Bicarbonate losses through GIT or kidneys
  (diarrhoe, intestinal fistulae, kidney diseases)
• Insufficient excretion of H in acute or chronic
  kidney failure and in some hereditary
  tubulopathies

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Severity of metabolic acidosis
pH HCO3
Light 7,35 7,30 22 20
Medium 7,30 7,20 20 16
Severe 7,20 7,10 16 10
Very severe lt 7,10 lt 10
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Anion gap
Ketones ? Lactate ? Other ?
AG
HCO3-
Cl-
Na
1 norma, anion gap 15 mmol/l 2 MAC,
bicarbonate ß ,chloride Ý , anion gap 15 mmol/l
3 MAC, bicarbonate ß ,chloride norm, anion gap
Ý
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Ketoacidosis during starvation

• Lipid catabolism
• Gluconeogenesis from oxalacetate, an important
  intermediate od Krebs cycle
• Accumulation of acetylcoenzyme A
• Ketonemia without hyperglycaemia
• Decreased albumin, phosphate depletion

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Diabetic ketoacidosis I(cell starvation)

• Nondiagnosed Type 1 DM, increased insulin demand
  during intercurrent diseases
• Hyperglycaemia
• Polyuria and dehydratation (glycosuria)
• Lipid degradation, gluconeogenesis, Krebs cycle
  blockade
• Ketonemia, ketonuria (instead of nitroprusside
  test specific b-hydroxybutyrate assay in blood,
  too)
• Kussmaul breathing, disturbed consciousness, coma
• Increased anion gap

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Diabetic ketoacidosis II(electrolyte disorder)

• Hyponatremia, hypophosphatemia
• Intracellular potassium depletion due to
• insulin deficiency
• outflow of K from cells (acidosis)
• Urinary losses of K (osmotic diuresis, RAA
  system activation in dehydration)
• Not always connected with hypokalemia
• Dangerous hypokalemia can occur during too rapid
  treatment with insulin
• FOLLOW IT!

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Ketoacidosis in alcohol, methanol and ethylene
glycol intoxication

• Ethanol Þ acetaldehyde, b-hydroxybutyrate (AG)
  and
• thiamin deficiency (coenzyme of pyruvate
  dehydrogenase)
• Hypalbuminemia, hypomagnesemia
• Tissue hypoxia (lactic acid)
• But vomitus leads to MAL
• Methanol Þ formaldehyde, formic acid (AG)
• Optic nerve (alcohol dehydrogenase)
• Ethanol as treatment
• Ethylene glycol Þ glyoxal, oxalic acid (AG)
• Acute tubular necrosis
• Treatment dialysis and ethanol

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Lactic acidosis

• Hypoxia (A) or block of degradation (B)
• A respiratory diseases, circulatory failure,
  anaemia. With RAC
• B some oral antidiabetics of biguanide type
  (withdrawn or strict indication
  contraindications), fructose, sorbitol
• B some malignancies, thiamin deficiency
  hereditary enzyme defects (G6PD)

• Norm lt 1,3 mmol/l
• gt 5 mmol/l high mortality

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Acidosis in kidney failure

• Simple principle decrease of glomerular
  filtration lt 0,3 ml/s (n 2 ml/s) the kidneys
  are not able to resorb bicarbonate and excrete
  acids
• Complicated reality adaptory mechanisms of
  tubuli / damage of tubuli
• Anion gap Ý phosphates Ý potassium Ý
• Dialysis

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MAC with normal anion gap(hyperchloremic)

• Bicarbonate losses through GIT (diarrhoe)
• Renal tubular acidoses
• RTA II proximal type
• RTA I distal type
• RTA III mixed
• RTA IV with hyperkalemia

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Acids and aldehydes

• Formic acid and formaldehyde, (from methanol)
• CH3OH Þ H2CO Þ HCOOH
• Acetic acid and acetaldehyde (from ethanol)
• C2H5OH Þ CH3-HCO Þ CH3-COOH
• Oxalic acid and glyoxal (from ethylene glycol
  antifreeze)
• HOCH2-CH2OH Þ OHC-CHO Þ HOOC-COOH
• Lactic acid (from glycolysis)
• CH3-CHOH-COOH
• b-hyrdroxybutyric, acetoacetic acid and acetone
  (stravation, insulin deficiency)
• CH3-CHOH-CH2-COOH, CH3-CO-CH2-COOH, CH3-CO-CH3

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Metabolic alkalosispH gt 7,45 HCO3- gt 26 mmol/l

• Decrease of extracellular space volume
• smaller space and increased K and H secretion
  due to activation of renin-angiotensin-aldosterone
  system, Na reabsorbtion, hypokaliemia
• Metabolites
• citrate from blood transfusions, milk alkali
  syndrome, metabolites of ketone bodies
• Mineralocorticoids Na retention, K and H
  depletion
• Chloride depletion diuretics, vomitus, Mg
  deficiency
• Dg. help Urinary chloride excretion lt or gt 10
  mmol/day

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Respiratory acidosis pH lt 7,35 pCO2 gt 5,8 kPa

• Connection between ABR and tissue oxygen supply
  remember haemoglobin dissociation curve
• CO2 in red cells is rapidly converted
  (carboanhydrase) to H2CO3 which dissociates to
  H and HCO3-
• Respiration is regulated by pH and pCO2
• RAC in respiratory disorders (as a part of
  global respiratory insufficiency) and in
  hemodynamic failure
• Renal compensation is not complete
• Tisue hypoxia leads to lactate acidosis

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Respiratory alkalosis pH gt 7,45 pCO2 lt 4,8 kPa

• Hyperventilation
• psychogenic, fever, G negative sepsis
• mountain disease, CO intoxication
• some drugs aminophyllin, salicylate
• some lungs diseases pulm. embolism
• Parestesia, cramps, arrhythmias (ionized Ca)