Transcript Prezentace aplikace PowerPoint

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
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Acidobasic balance (ABB) First of all ABB of
extracellular space – blood
7,4 = 40 nmol/l H+ (or 4*10-7 mol/l )
 (not H+ but H3O+)
CO2 production: 20 mols/day (300 – 360 l)
Strong (non-volatile) acid production: 60 – 70
mmols/day
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oxidation of SH groups (amino acids): sulfate
hydrolysis of proteins, phospholipids: phospate
keto acids, lactic acid...
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Logarithms
[H+]
Exp
pH
pH
nmol/l
mmol/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
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7,9
12
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Physiological a pathological values
Blood
Physical exercise
Frontiers of life
Urine
Red cells
Muscle cells
Bile
Duodenal juice
Prostata cells
Gastric juice
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pH
7,36 - 7,44
7,10
6,80 - 7,70
H+ nmol/l
44 - 36
94
158 - 20
4,50 - 8,00
32000 – 10
7,28
6,90
6,2 - 8,5
6,5 - 7,6
4,50
1,2 - 3,0
53
126
631 - 3
316 - 25
32 mmol/l
1000 - 63
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ABB
Measurement
Not very long ago...
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„Astrup”
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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
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Buffers only absorb the attacks of hydrogen ions and
prevent sudden big fluctuations of pH.
Closed systems
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hydrogencarbonate
phosphate
haemoglobin/protein
bones (carbonate)
Regulatory systems – open, regulate the
hydrogencarbonate system
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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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S im p le A B R diso rd e rs
a cid o sis
p H < 7 ,35
m e tab o lic
H C O 3 < 22
re sp ira to ry
C O 2 > 5 ,8
a lka lo sis
p H > 7 ,45
m e tab o lic
H C O 3 > 26
re sp ira to ry
C O 2 < 4 ,8
Acute and chronic
Not compensated, partial compensated, corriged
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Henderson and Hasselblach 1
metabolic acidosis – something is
decreasing bicarbonate (24)
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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 2
metabolic alkalosis – too much of
bicaarbonate
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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 3
respiratory acidosis – asfyxia
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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 4
respiratory alkalosis – histeria, mountain
sickness
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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
20 HCO3
MAC
RAC
MAL
RAL
1 CO2
7,4
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RAC, MAC, RAL, MAL
7,2
7,3
CO2
7,4
7,5
7,6
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HCO3
16
Compensation
7,2
7,3
CO2
7,4
7,5
7,6
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HCO3
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Compensated disorders
7,2
7,3
CO2
7,4
7,5
7,6
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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
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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+
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Metabolic acidosis
pH < 7,35; HCO3 < 22 mmol/l
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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
< 7,10
< 10
Very severe
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Ketones ?
Lactate ?
Other ?
Anion gap
15
25
AG
HCO3-
15
25
15
15
140
110
100
Na+
100
Cl-
1: norma, anion gap 15 mmol/l
2: MAC, bicarbonate  ,chloride  , anion gap 15 mmol/l
3: MAC, bicarbonate  ,chloride norm, anion gap 
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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)
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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
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insulin deficiency
 outflow of K+ from cells (acidosis)
Urinary losses of K+ (osmotic diuresis, RAA
system activation in dehydration)
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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 acetaldehyde, b-hydroxybutyrate (AG) and
 thiamin deficiency (coenzyme of pyruvate
dehydrogenase)
 Hypalbuminemia, hypomagnesemia
 Tissue hypoxia (lactic acid)
 But: vomitus leads to MAL
 Methanol  formaldehyde, formic acid (AG)
 Optic nerve (alcohol dehydrogenase)
 Ethanol as treatment
 Ethylene glycol  glyoxal, oxalic acid (AG)
 Acute tubular necrosis
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Treatment: dialysis andabre.ppt
ethanol
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Lactic acidosis
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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 < 1,3 mmol/l
> 5 mmol/l high mortality
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Acidosis in kidney failure
Simple principle – decrease of glomerular
filtration < 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  phosphates  potassium 
 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
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Formic acid and formaldehyde, (from methanol)
CH3OH  H2C=O  HCOOH
Acetic acid and acetaldehyde (from ethanol)
C2H5OH  CH3-HCO  CH3-COOH
Oxalic acid and glyoxal (from ethylene glycol “antifreeze”)
HOCH2-CH2OH  OHC-CHO  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 alkalosis
pH > 7,45; HCO3- > 26 mmol/l
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Decrease of extracellular space volume
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Metabolites
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smaller space and increased K+ and H + secretion due to
activation of renin-angiotensin-aldosterone system, Na
reabsorbtion, hypokaliemia
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. 17.7.2015
help: Urinary chloride excretion
< or > 10 mmol/day32
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Respiratory acidosis
pH < 7,35; pCO2 > 5,8 kPa
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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 HCO3Respiration 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 > 7,45; pCO2 < 4,8 kPa
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Hyperventilation
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psychogenic, fever, G negative sepsis
 mountain disease, CO intoxication
 some drugs – aminophyllin, salicylate
 some lungs diseases – pulm. embolism
Parestesia, cramps, arrhythmias (ionized Ca++)

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