Acid – base balance
Terms
• ICF = intacellular fluid
• ECF = extracellular fluid
• IVF = intravascular fluid
• EVF = extravascular fluid
Water
Body water
50-80 % of body weight (depending on age)
• 80 % - newborns
• 60 % - slim adults
• 55 % - obese adults
• 50 % - seniors
Body water distribution
Fluid
• ICF 40 % of body weight
• ECF 20 % of body weight
– Interstitial 15 %
– Intravascular 5 %
Body water distribution
Body – water distribution
Transcellular fluid
• Physiologically
– GIT (2-3 litres after food intake)
– CSF (cerebrospinal fluid)
• Patologically
• Abdominal cavity (ascites)
• Thoracic cavity (hydrothorax)
• Intestine (ileus)
• Bruises
Water balance
Intake (ml) Excretion (ml)
Drinking 1500 Urine 1500
Food 700 Perspiration 400
Nutrition oxid. 300 Breathing 400
Sweating 100
Faeces 100
Total 2500 2500
Can be measured Can be estimated
Water balance
Distribution of substances in water
1. Substances, which pass freely
through cell membranes
2. Substances, which make
concentration gradient (ICF x ECF)
3. Substances, which make
concentration gradient (IVF x EVF)
• Endogenous substances: urea
• Exogenous substances: ethanol
1. Substances, which pass freely
through cell membranes
Different concentration of these substances in ICF and ECF.
• Mainly ions (Na, K, Cl, Ca, Mg, P)
Mechanisms
• Semipermeable membrane (glucose)
• Iont pumps (active transport - Na/K ATPases, energy
required)
2. Substances, which make
concentration gradient (ICF x ECF)
Main ions
ECF (blood)
mmol/l
ICF (cells) mmol/l
Na 140 10
Cl 102 8
K 4,0 155
Ca 2,2 0,001
Mg 1,0 15
P 1,0 65
Different concentrations of substances in IVF and
EVF.
• Proteins (albumin)
• Proteins are responsible for keeping the water in
vessels
• Hypoproteinemia leads to edema
3. Substances, which make
concentration gradient (IVF x EVF)
Osmolality
• Osmolality = total amount of osmotic active
particles dissolved in one kg of water –
mmol/kg.
How to count osmolality
Plasma-osmolality (mmol . kg –1)
2[Na+] + [glucose] + [urea]
2 * 140 + 5 + 5 = 290 mmol . kg –1
Osmolal gap
• Difference between measured and counted
osmolality
OsmGap = POsmmeasured - POsmcalculated
• Discovers a presence of alcohol or etylenglycol
• If OsmGap > 10 mmol/kg , then presence of
these substances is very probable
• 1 g of ethanol in 1 litre of plasma (1 per mille of
alcohol) rises osmolality by 23 mmol/kg.
Regulation of osmolality
• Osmoreceptors
• Antidiuretic hormone (ADH) – regulates
resorption of pure water in kidneys
Hyperosmolality
Deficiency of water, many solutes
• Dehydratation
• fever, burns, inability of drinking
or
 concentration of glucose, urea, alcohol in
blood (osmotic active) but without
dehydratation
Reaction:  ADH → resorption of water in
kidneys, feeling thirsty
Hypoosmolality
Too much water and not enough soluts
• „overhydratation“
• too much infusions (glucose)
• Brain injury, defective secretion of
ADH
Reaction:  ADH, polyuria
Osmolality of urine
• 50 - 1400 mmol/kg H2O
– old people: max. 800
Ions
Ions in blood and cells
ECF (blood)
mmol/l
Cells mmol/l
Na 140 10
Cl 102 8
K 4,0 155
Ca 2,2 0,001
Mg 1,0 15
P 1,0 65
Main ions in blood
mmol/l
Na: 140
Cl: 102
HCO3: 24
Prot. 17
K Mg Ca
4 1 2,5
RA: 8
Na (sodium): 135 - 145 mmol/l
Distribution
• ECF 50 %
• Bone tissue 40 %
• ICF 10 %
Na ions are followed by water
Intake: NaCl (salt) 8-11 g/day (1 g/day is enough)
Excretion:
• urine: 120 - 240 mmol/l
• sweat: 10 - 20 mmol, faeces 10 mmol
Importance of Na: state of hydrataion, osmolality
Hypernatremia + loosing water
• Fever - sweating, hyperventilation
• Inability of drinking
Results:
•  osmolality → transfer of water from ICF to ECF
•  ADH -  water resorption in kidneys
Symptoms:  protein, hemoglobin, dehydratation,
hyperosmolality
Hypernatremia + increased intake of
Na
Intenstive infusion therapy
Results:
• hyperhydration
Symptoms: hyperhydration, polyuria
Hyponatremia
Too much of water
• Hyperhydration with glucose infusions
• Restriction of Na intake
Symptoms:
• edema, pulmonaly edema
• Encephalopathy
•  osmolality
Main ions in blood
mmol/l
Na: 140
Cl: 102
HCO3: 24
Prot 17
K Mg Ca
4 1 2,5
RA: 8
K (potassium): 3,7 - 5,1 mmol/l
Reserves 3 500 mmol, main iont of ICF
Distribution
• ICF 98 %
• ECF 2 %
Concentration
• plasma 3.7 - 5.1 mmol/l
• cells 110 - 160 mmol/l (ery 95 mmol/l)
Potassium - K
Excretion
• Urine: 45 - 90 mmol/24 hrs
• Faeces: 5-10 mmol/24 hrs
Sources – plant food
Importance: neuromuscular excitability,
related to pH in organism
Dependence of K on pH
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)
HyperK
• Decreased excretion by kidneys (oliguria, anuria)
• Transfer from cells to blood (acidosis, hemolysis,
katabolism)
Symptoms
• arrhythmia
• muscle weakness
Dangerous values:
• > 6,5 mmol/l
• > 9-10 mmol/l → ventricle fibrilation
• Requires HD (dialysis)
HyperK - therapy
If kidney are not affected by disease
• diuretics (furosemide i.v)
In case of renal insufficiency
• Infusion: glucose + insulin
• Ion exchanger (Resonium)
• dialysis
HypoK
• Increased excretion: diuretics, diarrhoea
• Low intake
• Transfer into cells (alkalosis, anabolism)
Symptoms:
• arrhythmia
• muscle weaknes, ileus
K - other
Blood exams K (red blood cells!)
• hemolysis (potassium washed up from cells to
plasma)
• samples have to be stored in fridge
Chlorides- Cl
Distribution
• Main iont of ECF 97 - 105 mmol/l
• ICF 3 - 10 mmol/l
Importance:
• osmolality
• Acid-base balance (change in concentration of Cl→
change in concentration of HCO3
- )
• gastric juices - HCl
Balance
• Excretion by urine 120 - 240 mmol/24 hrs
• Sweat 10 - 20 mmol, stolice 10 mmol/24 hod
Main ions in blood
mmol/l
Na: 140
Cl: 102
HCO3: 24
RA, Prot:
K Mg Ca
4 1 2,5
+ 

HyperCl
• Decreased excretion via kidneys
• Increased intake + renal insufficiency
• Increased intake of NaCl
Symptoms:
↑Cl- → ↓HCO3
- (buffer systém restricted –
inability of catching H+) → ↓ pH (acidosis)
HypoCl
Excretions
• Gastric juices (vomiting)
• Kidneys (diuretics, polyuria)
• Sweating
Symptoms:
↓ Cl- → ↑ HCO3
- (abundance of buffers), ↓ H+
→ ↑ pH (alkalosis)
Acid - base balance
pH: 7.35-7.45
• Activity of hydrogen ions
• Increased H+ = decrease pH.
• Low pH: blood is more acid
• High pH: blood is less acid
Acids and bases
Acids: release H+ iont
Bases: accept H+ iont
• Acids: lactate, carbonic acid
• Bases: bicarbonate
Normal pH: 7,35 – 7,45.
In case of deviation:
• Affects contractility of myocard, nerve conductance
• enzymatic functions
pH < 6,80 or > 7,80 is dangerous situation!
Deviations in pH
Keeping pH in normal ranges
3 systems:
• Extracelular buffers
• Lungs
• Kidneys
Acid – base balance
Normal pH: 7.35-7.45
Acidosis
• pH < 7.35
• Serious: pH < 6.80
Alkalosis:
• pH > 7.45
• Serious: pH  7.70
Keeping pH in normal ranges
Buffer bases
• React with acids and bases
• bind extra H+ ions (temporary solution)
Definitive solution = excretion of H+ ions by lungs or
kidneys.
Keeping pH in normal ranges
Main buffer systems:
Blood
• Natrium bicarbonate: NaHCO3
• Hemoglobin
• Proteins
ICF
• Phosphates
Bicarbonate buffer: NaHCO3
H+ + HCO3
-  H2CO3  CO2 + H2O
Lungs
Kidneys
HCO3
- resorption
Regeneration of
bicarbonates
Excretion of H+
Dissolving CO2 (carbon dioxide)
in blood
CO2 + H2O  H2CO3  H+ + HCO3
-
800 : 1 : 0.03
lungs(intensity of breathing - CO2 )
kidneys (excretion of H+, synthesis HCO3
-)
Bicarbonate (HCO3
-)
• Deficiency → acidosis
• Abundance → alkalosis
Compensation of acid-base
dysbalances
By:
• Lungs
• Kidneys
Pulmonary compensation
• Changing concentration of CO2 leads to
• Changes in contrentration of H2CO3
Pulmonary compensation
Metabolic acidosis: hyperventilation
• breathing out CO2,  H2CO3
• very effective mechanism
Pulmonary compensation
Matabolic alkalosis: hypoventilation
•  pCO2 ,  H2CO3 but  pO2, hypoxia
• not effective enough
Kidney compensation
Kidney compensation
Acidosis
•  synthesis of HCO3
•
 synthesis and excretion of NH4
+, H2PO4
-
Alkalosis
•  resorption HCO3
•
 synthesis of NH4
+ ( excretion H+), 
synthesis of HPO4
2-
AB dysbalance
• Acidosis
• Alkalosis
Metabolic
Respiratory (pulmonary)
Metabolic
Respiratory (pulmonary)
Combined AB dysbalance
Pulmonaly AB dysbalances
Respiration insufficiency
 Concentration of CO2
 Concentration of H2CO3
Acidosis
Excessive breathing
 Concentration of CO2
 Concentration of H2CO3
Alkalosis
CO2 + H2O  H2CO3 (carbonic acid)
Metabolic AB dysbalances
Too many acids
and/or
Low bicarbonate
Acidosis
Low amount of acids
and/or
Increased bicarbonates
Alkalosis
Concentration of acids and bases is changed
Metabolic acidosis
Accumulation of acids:
• ketoacids - diabetes
• intoxications (methanol, ethylenglycol etc.)
Loosing bicarbonates (diarrhoea)
Hyperchloridemia
Lactate acidosis
• Accumulation of lactate
•  utilisation of lactate (liver failure, metformin)
Metabolic alkalosis
Loosing chlorides
• Vomiting HCl (hydrochloric acid)
• diuretics
Increase of bicarbonates
• When treating acidosis
Respiratory acidosis
Accumulation of carbonic acid, when pulmonary
insufficiency (accumulation of CO2)
• Pulmonaly diseases (COPD), intoxications
leading to decreased respiratory centre
function
Respiratory alkalosis
Low carbonic acid when excessive breathing
(decrease of CO2)
• Hyperventilation syndrom (anxiety, stress)
• encephalitis, meningitis
Parameters
• pH Measuring of H+
• pCO2 respiratory part of AB balance
• HCO3
- metabolic part of AB balance
AG – anion gap
• Difference between main plasmatic cations
and anions (Na+ + K+) – (Cl- + HCO3
-)
• We can evaluate participation of lactate,
ketoacids etc. on AB dysbalance.
Compensation of AB dysbalance
Respiratory deviations are compensated by
kidneys and metabolic deviations are
compensated by lungs.
When to take Astrup
Metabolic disorders
• Ketoacidosis, diabetes mellitus
• Intoxications
• Mineral dysbalances
Respiratory disorders
• Respiratory insufficiency
• COPD
Taking blood sample
• MD is responsible
• Taken from artery, without acess of the air
Save the 1st patient
• Patient is vomiting several days. What are the
expected changes in AB balance?
• Answer: hypochloremic metabolic alkalosis
(loosing hydrochloric acid)
• Because patient is really sick, he is starving.
What are the expected changes in AB
balance?
• Answer: metabolic ketoacidosis.
Type of AB dysbalance
• Combination of metabolic acidosis and
metabolic alkalosis
Save the 1st patient
• What about pH? Will it be deviated or in
normal ranges?
• Which biochemical parameters should be
examinated?
Save the 1st patient
Save the 1st patient
- how to treat him?
Stop vomiting
• Antiemetic medication (metoclopramid/itoprium
chlorid/ondansetron)
Rehydration
• Infusion with NaCl (substitution of Cl), glucose
infusion (nutrition)
Nutrition
• Parenteral / later enteral
Save 2nd patient
• Patient with DM is not compliant and he
decided not to take his insulin regularly. What
are the expected changes in AB balance?
• Answer: hyperglycemia → ketoacidosis
Hyperglycemia → osmotic diuresis → polyuria
and dehydration (hypovolemia) → tissue
hypoxia → lactate acidosis
Type of AB dysbalance
• Combination of two metabolic acidoses
(ketoacidosis from DM+ lactate acidosis from
tissue hypoxia)
Save the 2nd patient
- how to treat him?
• Treat the DM properly
• Insulin + rehydration, regular controls of
potassium (beware of hypokalemia during
treatment of hyperglycemia).
• Decrease glycemia slowly (brain edema).
Save 3rd patient
• Patient with cardiopulmonary arrest. What are
the expected changes in AB balance?
• Answer: respiratory acidosis (CO2 is rising up
in organism)
+
• Tissue hypoxia → lactate acidosis
Type of AB dysbalance
• Combination of respiratory acidosis and
metabolic acidosis.
Save the 3rd patient
- how to treat him?
• CPR
• Artificial ventilation
• …