Acid – base balance
Ondrej Kyselak, MD, PhD
Dept. of Clinical Biochemistry, St. Anne's University Hospital Brno
Dept. of Laboratory Methods, Faculty of Medicine, Masaryk University
Homeostasis, compartments
• Blood plasma
• Interstitial fluid
• Intracellular fluid
Functions:
• transport of nutrients, oxygen, hormones, antibodies
• transport of catabolites, CO2, hormones
• cell migration (cellular immunity)
• maintenance of pH, osmolality and ionic composition
• temperature stability
Body water
Human body contains approx. 50-80 % of water
(depending on age)
• 80 % - newborns
• 60 % - adults
• 50 % - elderly people
Distribution of water in the body
• Intracellular (ICF) 40 % body weight
• Extracellular (ECF) 20 % body weight
Interstitial 15 %
Intravascular 5 %
Transcellular fluid
Physiologically
• GIT (after eating 2-3 liters)
• Cerebrospinal fluid (CSF) 120 -180 ml in adults
Pathologically
• Abdominal cavity (ascites)
• Thoracic cavity (hydrothorax)
• Intestine (ileus)
• Hematomas
Water balance
Intake (ml) Excretion (ml)
Drinking 1500 Urine 1500
Food 700 Perspiration 400
Oxidation of
nutrients
300 Breath 400
Sweat 100
Faeces 100
Total 2500 2500
Can be measured Can be estimated
Osmolality
The ratio of water to all dissolved substances,
regardless of their size.
Normal ranges: 280 - 300 mmol/kg H2O
Influenced by concentration of Na+, urea, glucose
Calculation of plasma osmolality
(approximately)
2[Na+] + [Glucose] + [Urea]
2 * 140 + 5 + 5 = 290 mmol . kg –1
Osmolal gap
• Difference between measured and calculated
osmolality
OsmGap = POsmmeasured - POsmcalculated
• Detection of the presence of volatile substances
(alcohol, ethylene glycol)
• If OsmGap > 10 mmol/kg, the presence of volatile
substances is very likely
• 1 g of ethanol per litre of plasma (1 per mille of
alcohol) increases osmolality by about 23 mmol/kg.
Regulation of osmolality
• Osmoreceptors
• Antidiuretic hormone (ADH) – regulation of
clean water excretion in the kidneys
Hyperosmolality
Lack of water, many solutes
• Dehydration
• Temperatures, burns (loss of clean water),
inability to drink (reduced intake of clean water)
or
•  concentration of substances in the blood
(glucose, urea, alcohol) but without dehydration
Reaction:  ADH secretion → increase in resorption
of clean water in the kidneys (a decrease in urine
production that will be more concentrated) + feeling
thirsty
Hypoosmolality
Too much of water and lack of solutes
• „Poisoning with the water“
• Inappropriate infusion treatment (glucose)
• Brain injury, ADH oversecretion
Reducing the concentration of substances in the blood
(Na+, albumin, proteins) → risk of water leakage into
interstitium and the development of edema
Reaction:  ADH secretion and increase in production of
urine that will be less concentrated
Osmolality in urine
50 - 1400 mmol/kg H2O
• in old age: max. 800 (decreased renal
concentration capacity)
It depends on:
• renal concentration capability
• diuresis (water intake)
Hydration disorders
Natrium and water are regulated together.
However, the organism reacts differently to the
loss or excess of clean water and water with
solutes.
Like a pond...
• Clean water
• Solutes (Na+) are fish
Hydration disorders
Hydration dysbalance appears as a result of an
excess or lack of:
• Clean water
• Water with solutes (water + Na+)
Basic rules
• The resulting disorder depends on the type of
missing / excess fluid
• Accordingly, the body reacts by activating the
appropriate regulation system
• Natrium is osmotically active. The water
follows Na+.
Basic rules
The body regains what it has lost and gets rid of
what it has excess
• Loses clean water, resorbs clean water... (ADH)
• Loses water with solutes, resorbs water with
solutes... (aldosterone)
And vice versa... has an excess of water with
solutes, excrets water with solutes (natriuretic
peptide)
Basic rules
Hydration disorders (dehydration and hyperhydration) are
divided according to what the resulting disorder is, i.e.
whether it leads to:
• Isoosmolality – isotonic hyper/hypohydration
• Hypoosmolality – hypotonic hyper/hypohydration
• Hyperosmolality – hypertonic hyper/hypohydration
... not depending on which fluid is lost or dwells (isotonic,
hypotonic or hypertonic).
Basic rules
The organism has 3 basic control systems that affect the
metabolism of clean water or water with solutes:
• ADH - clean water resorption
• Aldosterone – resorption of Na+ which is followed by water
• BNP (natriuretic peptide) – inhibits Na+ resorption leading
to natriuresis. Na+ is followed by water.
Changes in the volume of clean water
Loss of clean water
→ hypertonic dehydration
Hypertonic dehydration
Loss of clean water → increase in osmolality
• Causes: insufficient water intake (elderly people),
unconsciousness, polyuric phase of renal failure – loss
of low concentrated urine, diabetes insipidus.
• Consequences: ↑ concentration of Na+ in ECT and
osmolality
• Reaction: clean water is missing → clean water must be
resorbed (ADH system used). Activation of
osmoreceptors in the hypothalamus, ↑ ADH and
increase the resorption of clean water.
Excess clean water
→ hypotonic hyperhydration
Hypotonic hyperhydration
Excess clean water → decrease of osmolality
• Causes: inability to excrete clean water (cardiac
patients, oliguria / anuria). Rarely "water poisoning",
SIADH (syndrome of inadequate ADH secretion),
tumors, brain damage. Excessive water resorption
occurs, urine is hyperosmolal.
• Consequences: hypoNa and hypoosmolality,
• Reaction: ↓ ADH, production of unconcentrated
urine
• Treatment: restrictions on water intake.
Changes in water volume with solutes
Loss of isoosmolar fluid
→ isotonic dehydration
Isotonic dehydration
Loss of isotonic fluid (water + Na+)
• Causes: vomiting, bleeding, burns, shock
• Consequences: osmolality does not change, haemoconcentration is
present, rise of haemoglobin and protein concentrations.
• Reaction: osmoreceptors do not react. Organism reacts when BP
decreases and renal perfusion is reduced. Activation of the
juxtaglomerular apparatus of the kidneys and secretion of renin
(centralization of circulation).
• Renin → angiotensinogen → angiotensin I, which, using ACE is
converted into angiotensin II → angiotensin III (peripheral
vasoconstration and aldosterone production) – ↑resorption of Na+
which is followed by the water
Excess isoosmolar fluid
→ isotonic hyperhydration
Isotonic hyperhydration
Excess isotonic fluid (water + Na+)
• Causes: cardiac failure, hypoproteinemia (nephrotic syndrome).
• Consequences: osmolality does not change (↑ water and Na+),
ECF volume is increasing. The development of oedema in
hypoproteinemic patients (fluid moves to extravasal
compartment) → reduced volume of circulating fluid in blood
vessels activates RAAS → secondary hyperaldosteronism.
• Reaction: secretion of natriuretic peptides (BNP) from LA and LV
in response to increased preload of the heart. Osmoreceptors
don‘t react. Inhibition of Na+ resorption in the distal tubule →
natriuresis with the water excretion.
Acid-base balance
pH definition
Def.: pH is a negative decimal logarithm of
activity (concentration) of hydrogen cations.
pH = -log10[H+]
pH stability in the organism
• pH is strictly regulated (pH = 7,35 – 7,45)
• pH < 6,80 or > 7,80 is dangerous!
• pH stability is necessary to maintain the stability of the
homeostasis
• Distribution of substances in the organism, ion and
water balance, pH optimum of enzymes, changes in
protein structure when pH changes, etc.
• pH stability is a priority needed to survive, therefore
effective compensatory mechanisms are available:
buffers, kidneys, lungs (+ liver activity – urea synthesis)
Maintaining physiological pH
3 systems:
• Extracellular buffers1)
• Lungs2)
• Kidneys2)
---
1) primary quick compensation
2) secondary slow compensation
AB dysbalance
Acidosis
• pH < 7,35
• Severe… pH < 6,80
Alkalosis:
• pH > 7,45
• Severe… pH  7,70
Basic AB disorders
• Acidosis
• Alkalosis
Metabolic
Respiratory
Metabolic
Respiratory
+ combined AB disorders
Metabolic acidosis - causes
Acid accumulation:
• Ketosubstances - starvation, diabetes
• Acid metabolites - renal failure
• Poisoning (methanol, strong acids)
Loss of bicarbonate (diarrhea) or ↑chloridemia
Lactate acidosis
• overproduction of lactate
•  lactate utilization (liver failure, sepsis, biguanide
poisoning)
Metabolic alkalosis - causes
Chloride loss:
• Vomiting HCl (hypoCl MAlk)
• Nasogastric tube – suction of gastric juices
• Diuretics
Excess bicarbonate
• Overdose in the treatment of acidosis
Respiratory acidosis - causes
Accumulation of carbonic acid in insufficient
breathing (CO2 accumulation)
• diseases of the lungs, diaphragm, respiratory
nerves, respiratory center (drug poisoning!)
Respiratory alkalosis - causes
Lack of carbonic acid due to excessive breathing
(decrease in CO2)
• Hyperventilation syndrome (anxieta, hysteria,
stress)
• Cerebral lesions (encephalitis, meningitis,
tumors, trauma)
• Pulmonary embolization
Maintaining a normal pH
Limiting the influence of acids and bases using the
buffers
• Reaction with acids, bases
• Maintaining physiological pH
• Binding excess H+ ions (temporary solution)
Permanent solution = excretion of H+ ions by the
lungs and/or kidneys
Main buffers
Blood
• Sodium hydrogen carbonate: NaHCO3
• Hemoglobin
• Proteins
Intracellular fluid
• Phosphates
Hydrogencarbonate buffer
H+ + HCO3
-  H2CO3  CO2 + H2O
• Synthesis in the kidneys
• Blood concentration: 24  2 mmol/l
Dissolution CO2 in the blood
CO2 + H2O  H2CO3  H+ + HCO3
-
800 : 1 : 0.03
Lungs (intensity of exhalation CO2 )
Kidneys (excretion of H+, synthesis HCO3
-)
Hydrogencarbonate (HCO3
-)
• Deficiency (decrease in concentration) → acidosis
• Excess (increase in concentration) → alkalosis
Compensation of AB dysbalances
The compensation of alkalosis and acidosis (the
body's reaction to deflection) takes place in the
opposite way to the one that triggered the
pathological condition.
Respiratory disorders are compensated
metabolically (by the kidneys) and vice versa.
Pulmonary compensation
Change in the pCO2 → change in concentration
of H2CO3
Pulmonary compensation
for metabolic acidosis
Reaction: hyperventilation, Kussmaul's breathing
exhalation CO2,  H2CO3
• effective mechanism
•
Pulmonary compensation for metabolic
alkalosis
Reaction: hypoventilation
 pCO2 ,  H2CO3 but  pO2, hypoxia
• low-effective mechanism
•
Kidneys
HCO3
- returned to blood
Bicarbonate regeneration
Exclusion
hydrogen ions
Kidney compensation
Acidosis
•  synthesisHCO3
•
 synthesis and excretion NH4
+, H2PO4
-
Alkalosis
•  resorption HCO3
•
 synthesis NH4
+ ( exkrece H+),  synthesis
HPO4
2-
AB balance parameters examination
• pH Measurement H+
• pCO2 Measurement of the resp. component
• HCO3
- Measurement of metabolic component
AB balance parameters
Anion gap (AG)
• difference between the main cations and plasma
anions (Na++K+) – (Cl-+HCO3
-)
• is used to assess the proportion of lactate,
ketosubstancces, oxalate in the AB disorder.
Strong ion difference (SD)
• (Na++K++Ca++Mg+) - Cl•
used to assess Cl ions on the AB dysbalance
When to examine AB balance
parameters
Metabolic disorders
• Metabolic disorders (ketoacidosis, DM not well
compensated)
• Poisoning drugs
• Ion dysbalance
Respiratory disorders
• Respiratory insufficiency
• COPD
Taking the blood sample
• The sample is taken from the artery without
the access of the air
Selected ions and their
relationship to AB dysbalance
Ions in blood and cells
ECF (blood)
mmol/l
ICF (cells) mmol/l
Na 140 10
K 4,0 155
Cl 102 8
Ca 2,2 0,001
Mg 1,0 15
P 1,0 65
Cations (mmol/l)
Na+ 140
Anions (mmol/l)
Cl- 100
K+ 4,5
Ca2+ 2,5
Mg2+ 1,0 RA- 8
P- 2,0
Prot. (albumin)- 11
HCO3
- 24
The most significant ions in connection
with AB dysbalance
• Potassium
• Chlorides
• Calcium
Potassium
• Physiological concentration K = 3,7 - 5,1
mmol/l
• Main ICF ion (98 % protein binding and
polysaccharides), stock about 3 500 mmol
Concentration
• plasma 3,7 – 5,1 mmol/l
• cells 110 - 160 mmol/l (ery 95 mmol/l)
→ in strongly hemolytic samples we do not
measure the concentration of potassium.
Potassium
Source: plant-based diet
Losses
• Urine: 45 - 90 mmol/24 hrs
• Faeces: 5-10 mmol/24 hrs
Fundamental relationship to the pH of the
organism.
K-pH dependency
1
2
3
4
5
6
7
8
9
6,9 7 7,1 7,2 7,3 7,4 7,5 7,6 7,7
pH
K(mmol/l)
K+H+
H+
H+
H+H+
H+
H+
H+
H+
H+
K+
K+
K+
K+
K+
K+
K+
H+
H+
K+
K+
K+
K+
H+
H+
H+
H+
K+
K+
K+
H+
H+
H+
H+
H+
H+H+
H+
H+
H+
H+
H+
H+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
H+
Acidosis (↑[H+] → ↓pH)
Increase in extracellular
concentration of H+. H+
move into the cell in
exchange for K+ →
hyperkalemia
Alkalosis (↓[H+] → ↑pH)
Reduction of extracellular
concentration H+ opposite
process→
hypokalemia
Attention!
• Decompensated diabetics experience diabetic
ketoacidosis and hyperkalemia (see the mechanism
above).
• When you start to treat the diabetes, the situation
reverses (K+ returns to the cell, and H+ out). In the
meantime, however, due to osmotic diuresis
(hyperglycaemia), a significant amount of K+ leaves the
urine → hypokalemia
While treating the diabetes, it is necessary to check the
ions and substitute eventual hypokalemia
Hyperkalemia
• Increased intake (also iatrogenous)
• Reduced renal excretion (oliguria, anuria)
• K+ is leaving the cells when: acidosis, haemolysis,
catabolism.
Symptoms
• Arrhytmia
Dangerous values:
• > 6,5 mmol/l
• > 9-10 mmol/l → ventricular fibrillation
• HD is required
Hyperkalemia - treatment
Treatment in the patients with functional kidneys:
• Diuretics (furosemide)
Treatment if renal failure
• Glucose infusion with insulin (insulin promotes
glucose entry into cells together with K+)
• Ion – Exchange (Calcium Resonium - CaR)
• Hemodialysis
Calcium Resonium (CaR)
• Contains calcium polystyrene sulphonate
• Redundant K+ is exchanged in the body for
Ca2+ (especially in the large intestine). CaR
resorption to systemic circulation does not
occur
• Redundant K+ is excreted by faeces
• KI: ileus, hyperCa, hyperPTH,
multiple myeloma, K < 5 mmol/l
Hypokalemia
• Increased losses: diuretics, GIT causes
(diarrhoea)
• Reduced intake (long-term)
• Move into the cells (alkalosis, anabolism)
Symptoms:
• Arrhythmia
• Muscle weakness, ileus
Hemolysis
Examination K+ (erythrocytes!)
• watch out for hemolysis (ery contain a lot of
potassium)
Chlorides - Cl
• Physiological concentration 97 - 105 mmol/l
• Main anion of ECF
• ICF 3 - 10 mmol/l
Function:
• osmolality
• maintaining AB balance (change in concentration Cl- → change in
concentration HCO3
- )
• gastric juice - HCl
Intake in NaCl
Losses
• Urine 120 - 240 mmol/24 hrs
• Faeces 10 mmol/24 hrs, sweat 10 - 20 mmol
Hyperchloridemia
• Reduced excretion — renal disease
• Increased intake (NaCl) in renal disease
• Increased NaCl by iatrogenous supply (cave
FR)
↑Cl- → ↓HCO3
- (buffering system limited – is
unable to bind H+) → accumulating H+ → ↓ pH
(development of acidosis)
Cations (mmol/l)
Na+ 140
Anions (mmol/l)
Cl- 100
K+ 4,5
Ca2+ 2,5
Mg2+ 1,0 RA- 8
P- 2,0
Prot. (albumin)- 11
HCO3
- 24
Anions (mmol/l)
↑ClRA-
8
P- 2,0
Prot. (albumin)- 11
↓HCO3
-
Hyperchloridemia
Hyperchloridemic metabolic acidosis
• Beware of long-term saline therapy (when
hyperNa, hyperCl do not give more) – a more
suitable is glucose infusion if there is no
contraindications
• HyperNa (water movements), hyperCl (MAc)
Hypochloridemia
Losses
• Gastric juice (vomiting, suction by NGT)
• Kidneys (diuretics, polyuria)
• Excessive sweating
↓ Cl- → ↑ HCO3
- (buffering system in excess), ↓
H+ (bound with buffer) → ↑ pH (development of
alkalosis)
Cations (mmol/l)
Na+ 140
Anions (mmol/l)
Cl- 100
K+ 4,5
Ca2+ 2,5
Mg2+ 1,0 RA- 8
P- 2,0
Prot. (albumin)- 11
HCO3
- 24
Anions (mmol/l)
↓ClRA-
8
P- 2,0
Prot. (albumin)- 11
↑HCO3
-
Hypochloridemia
Hypochloridic metabolic alkalosis
• Patients with dyspepsia and vomiting
• Suction of gastric juices by NGT
Calcium
• The largest depo in the bones (1,2 kg in the form of
hydroxyapatite)
Ca in the blood:
• Ca bound to proteins (undiffusible), mainly albumin
(46 %)
• Ca free, ionized1) (48 %) – biologically active fraction
• Ca in complex compounds1) (6 %), citrates,
phosphates, lactate, sulfate
Function: nerves, formation of bone mass
---
1) Diffusible forms of Ca
Total vs. ionized calcium
Total calcium is the sum of:
• Ca ionized (cca 1/2 of total Ca)
• Ca protein-bound (mainly albumin)
• Ca bound to complex compounds
Ionized calcium
• Only ionized Ca has physiological effects
(hypo/hyperCa symptoms therefore occur when this
fraction changes)
• Hypoalbuminemia → reduced concentration of total Ca
(but normal levels of ionized Ca are often present,
therefore the patient may not have typical symptoms).
Together with the total calcium, ionized calcium should
be examined as well
Calcium
• Physiological concentration: 2,1 - 2,6 mmol/l
• Strict regulation in the organism (very strict
reference range)
• Relatively small dysbalance can lead to potential
life-threatening conditions
Ca protein binding
Affected by:
• Protein concentrations, in particular albumin
(hypoalbuminemia → ↓total Ca)
• pH value
✓ Acidosis → Ca release, free fraction increase
✓ Alkalosis → Ca binding, decrease in free
fraction
Changes in calcemia in AB dysbalances
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
H+
H+
H+
H+
H+
H+
H+
H+
Ca2+
H+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
H+
H+
H+
H+
H+
H+
H+
H+
H+
H+
H+
H+
H+
H+
H+
Acidosis
Alkalosis
Ca changes in different situations
• Albumin decrease of 10 g/l = Ca decrease of 0.25 mmol/l
• decrease Ca
✓ drugs (furosemid, bisphosphonates)
✓ hyperP, hypoMg
✓ malabsorption, kidney disease, tumours
Changes to AB balance
• pH decrease (acidosis) → hyperCa
• pH increase (alkalosis) → hypoCa
Sampling kits: not into tubes with EDTA or Na-citrate (they bind Ca)
Regulation of Ca levels in the blood
• Calcitonin – parafolicular cells if thyroid gland,
reduces Ca levels in the blood
• Parathormon (PTH) – increases Ca levels in
the blood (by releasing from the bones,
increases reabsorption of Ca in the kidneys,
stimulates the formation of calcitriol in the
kidneys)
• Vitamin D (active form – calcitriol) – support
for resorption of Ca from the intestine
Hypocalcaemia
Causes:
• Long-term depletion Ca
• Absorption disorder: vitamin D deficiency (lipophilic vitamin,
malabsorption syndromes)
• Parathormone deficiency (iatrogenously, when the thyreoidectomy
may accidentally remove the parathyroid glands) – a necessary check
of Ca and PTH after surgery.
Symptoms:
• Paresthesia
• Tetany, arrhythmia
• Dyspnoea
Phase of AP of the heart muscle fibers
(changes in membrane conductivity for individual ions)
• 0 - depolarisation
• 1 - initial rapid repolarization
• 2 - plato phase
• 3 - late rapid repolarization
• 4 - resting potential
The plato phase (2) is triggered by a
slow opening VOC Ca2+ (–30 až –40 mV)
The final repolarization (3) on the
resting potential (4) is the closure of
VOC Ca2+.
AP and mechanical response of heart
muscle fibers
ARP – absolute refractory period
RRP - relative refractory period
• During phases 0-2 and half of
phase 3, the heart muscle
cannot be re-excitated (ARP).
The RRP then takes until phase
4.
• Therefore, unlike skeletal
muscle, tetany (under
physiological circumstances)
cannot be developed in the
heart muscle → protection from
malignant arrhythmia.
Strict regulation of Ca in the body is
absolutely crucial
• Ca2+ ions play an essential role in maintaining
ARP. HypoCa may lead to cardiac muscle
tetany and life threatening arrhythmias
• The need to maintain an optimal pH with
regard to Ca concentration protects from
malignant arrhythmia
Hypercalcaemia
Causes:
• Increased absorption (excess vitamin D)
• Excess parathormone (adenomas parathyreoid
glands)
Symptoms:
• Myasthenia
• Nausea
• Polyuria
Another ions (Na, P, Mg) + RA
Minimal relationship to AB balance influence
• Na – deviations lead to water dysbalance
• P – phosphates affect Ca concentration product
[Ca] x [P] = konst.
• Mg – nerve irritation
RA = residual anions (S, organic acids)
Sodium
Physiological concentration: 135 - 145 mmol/l
• ECF 50 %
• Bone tissue 40 %
• ICF 10 %
Na is osmotically active → water binding (retention Na
→ water retention).
Intake NaCl 8-11 g/day (however, 1 g/day is sufficient)
Losses:
• Urine: 120 - 240 mmol/l
• Sweat: 10 - 20 mmol, faeces 10 mmol
Meaning of examination Na: hydration, osmolality
Sodium
• Na+ has an essential relationship to
influencing the distribution and balance of
water
• The relationship with AB balance is negligible
• Concentration disturbances Na+ → water
management disorders (hyper/dehydration)
• 3 regulatory systems: ADH, aldosterone,
natriuretic peptide
Phosphorus
• Stock 600 g (85 % - bones, 15 % - soft tissues)
• Main ion of ICF: organic phosphates
(phospholipids, phosphoproteins, ATP, nucleic
acids)
• Inorganic phosphates (serum - mono and
dihydrophosphate, protein binding, P –
buffer), hydroxyapatite in the bones
Fluctuations in phosphatemia
• Increase - chronic renal failure
• Reduction - absorption disorders, antacids
Calciophosphate product
[Ca] x [P] ≤ 4,4 mmol2/l2
Increased product Ca x P in plasma:
• Leads to the precipitation of calcium salts in soft
tissues → HypoCa
• Inorganic P inhibits 1-hydroxylation → reducing
creation 1,25-dihydroxyvitamin D →↓ resorption of Ca
in the intestine → HypoCa
In patients with CKD who are supplemented with vitamin
D(↑ Ca) ectopic calcification is a common complication if
hyperphospatemia correction is not sufficient.
Magnesium - Mg
• 55 % in the bones (25 g)
• 45 % intracellular (main ICF ion - ATP, GTP)
• Blood
✓30 % protein binding
✓55 % ionized fraction
✓15 % complexes: citrates, phosphates, other
anions
• Function: nervous-muscle irritation, bone mass,
enzyme cofactor. In the context of AB balance
minimal importance.
Residual anions
• RA includes organic acids
• Lactate (product of anaerobic glycolysis –
examination is commonly available in the labs)
– respiratory arrest, shock, post-resuscitation
conditions, biguanides (metformin), etc.
• Ketosubstances (acetoacetate, βhydroxybutyrate,
aceton)
Production of ketosubstances during
the decompensation of DM
Absolute (DM1) / Relative (DM2) Insulin deficiency
↓
Glucose entry failure in cell → hyperglycaemia
↓
Instead of glucose, cells utilize FA (β-oxidation)
↓
Production of ketosubstances →↓pH
↓
Diabetic ketoacidosis (complications - DM coma)
Cations (mmol/l)
Na+ 140
Anions (mmol/l)
Cl- 100
K+ 4,5
Ca2+ 2,5
Mg2+ 1,0 RA- 8
P- 2,0
Prot. (albumin)- 11
HCO3
- 24
Anions (mmol/l)
Cl- 100
↑ RAP-
2,0
Prot. (albumin)- 11
↓HCO3
-
Combined AB disorders (1)
The patient vomits for several days. What
changes can I expect in ABB?
• Loss of HCl → hypochloridemic MAlk
+
Due to nausea, the patient starves and does not
want to receive food.
• β-oxidation of FA → production of
ketosubstances → metabolic ketoacidosis
Development of combined AB disorder
Type of AB disorder
• Combination of metabolic acidosis and
metabolic alkalosis
• pH can be normal, only pH is not enough to
investigate
• The proportion of ions must be determined (in
particular Cl-) on AB disorder → always
examine the ions!
Combined AB disordes (2)
Non-compliant patient, diabetic who forgets to
inject insulin. What changes can I expect in ABR?
• Hyperglycemia → β-oxidation of FA → DM
ketoacidosis
+
• Hyperglycemia → osmotic diuresis → polyuria
and dehydration (hypovolaemia) → tissue
acidosis → lactic acidosis
Type of AB disorder
• Combination of two metabolic acidosis
(ketoacidosis from DM + lactic acidosis from
tissue hypoxia)
Combined AB disorders (3)
Patient with CP arrest. What changes can I
expect in ABR?
• Increase of CO2 due to respiratory
insufficiency → respiratory acidosis
+
• Tissue hypoxia → lactic acidosis
Type of AB disorder
• Combination of respiratory acidosis and lactic
acidosis
Take home message
• The stability of pH is a prerequisite for maintaining
physiological processes in the organism
• ABB disorders are associated with the movement of ions
between the compartments as well as with changes in their
concentrations
• K+, Cl-, Ca2+ have a significant relationship to ABB disorders
(K+ /pH dependency, Cl- /HCO3
- and Ca2+/pH relationship)
• Na+, P-, Mg2+ dysbalances are primarily associated with
other disorders (transfer of the water between
compartments, neuromuscular excitability etc.)
• Residual anions – their contribution to ABB disorders is very
important and should be clarified as well
Take home message
• In case of AB dysbalances the basic ions should
be examined: Na, K, Cl + better Ca, P, Mg.
Without this, (especially combined ABB
disorders) cannot be evaluated at all.
• The measurement of lactate should be performed
(it has a contribution to lactic acidosis)
• Beware of hypokalemia when compensating DM,
hyperglycemia should be trated very slowly
(changes of K+ when pH changes) + brain edema
• Do not forget to examine the ionized Ca
(biologically active form)