Transcript Acid –Base Balance - Dr

Acid –Base Balance
Adedapo K.S.FWACP( Lab. Med.)
BASIC CONCEPTS OF HYDROGEN
ION HOMOEOSTASIS
Metabolic processes in the body lead to
the production of hydrogen ions which, if
left to accumulate, would be injurious to
the body
 The body, therefore, has a number of
ways to remove the hydrogen ions
produced to provide a conducive
environment for cellular processes to
continue.
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Sources of Hydrogen ions
Conversion of amino acid nitrogen to
urea releasing equimolar amounts of
hydrogen ions.(H+)
 Anaerobic carbohydrate metabolism
yields lactate and H+
 Anaerobic metabolism of fatty acids and
ketogenic amino acids yield acetoactate
and also equimolar amounts of H+.
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Definitions
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Acid: An acid is a compound which dissociates in an
aqueous solution to produce hydrogen ions.
e.g. HCl H+ + CLBase: A base is a substance that is capable of
accepting hydrogen ion.
e.g. HCO3- + H+  H2CO3
Buffering: Buffering is the process by which a strong
acid (or base) is replaced by a weaker one with a
consequent reduction in the number of free hydrogen
ion(H+). The essence of a buffer is to mop up H+ and
produce a minimal change in pH.
H+ Cl- + NaHCO3  H2CO3 + NaCl
strong acid Buffer
weak acid neutral salt
Buffer
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Buffer. A buffer is the salt of a weak acid
which, when exposed to high H+ concentration
of a strong acid, forms a weak acid.
 pH. is a measure of hydrogen ion activity. It is
log10 of the reciprocal of the hydrogen ion.
 The log10 of a number is the power to which
10 must be raised to produce that number.
 pH of the blood is 7.35-7.45
Henderson-Hasselbalch Equation
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It expresses the relationship between pH and
a buffer pair. In aqueous solution, the pH is
determined by the concentration ratio of the
acid to its conjugate base.
pH = pK + log (HCO3-)
(H2CO3)
pK is the log of dissociation constant K
Henderson’s equation
H2CO3 is in equilibrium with dissolved
CO2 and so can be inserted into the
equation in place of H2CO3 which cannot
be measured directly.
 Substituting (Co2) in place of H2CO3 in
the previous equation;
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pH= pK + log(HCO3-)
(CO2)
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Henderson’s equation
pK for HCO3/H2CO3 buffer pair is 6.1
 pCO2 in kilopascals is 0.23, and 0.03 in
mmHg.
 Putting this back in the equation
 pH = 6.1 + log (HCO3-)
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PCO2x 0.23
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Control of Carbon dioxide (CO2)
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Control of CO2 is by the lungs
The lungs participates in the maintenance of H+ ion
when:
 Inspired oxygen is carried from the lungs to tissue
by haemoglobin.
 The tissue (cells) use the oxygen
 for aerobic metabolism and release CO2.
 CO2 diffuses along a concentration gradient from
the cells into the extracellular fluid and is returned
by the blood to the lungs where it is eliminated in
the expired air.
Buffer Pairs in body system
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Central to maintenance of the steady state of
pH is the HCO3-/H2CO3 buffer pair. Other
buffer pairs / systems are:
·Protein- /protein
· Hb-/HHb
· NH3-/NH4 pk=9.8
· NaHPO4-/NaH2PO4 pK=6.8
A buffer pair functions best at pH nearest
its pK
HCO3-/H2CO3 buffer pair
Workhorse of the buffering Process
 Accounts for most of the buffering in the
steady state
 2 main mechanisms
 Bicarbonate resorption and
 Bicarbonate regeneration
 Regeneration in the Kidney and
erythrocytes
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Bicarbonate Resorption
Result: No net gain of HCO3, Most useful in steady state
HCO3 Generation
There is net gain of HCO3
Bicarbonate Generation by Erythrocytes
Here Hb serves as the blood buffer Hb-/HHb
Red Cell
Urinary buffers
These do not operate separately from
the above mechanism, but are, however,
brought into play when bicarbonate
concentration becomes reduced in
acidotic states.
 The two most important ones are
phosphate and ammonia.
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Urinary buffers
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Ammonia is produced during the deamination
of glutamine in the renal tubular cells, The
enzyme glutaminase catalyses the reaction
which is itself triggered off by the state of
acidosis, thereby allowing the generation of
the required ammonia which readily diffuses
across the renal tubular cell.
 NH3 + H+ -- NH4
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The ammonium ion (NH4) so formed is
passed out in the urine, thus promoting the
loss of excess H+ ions and reducing acidosis.
Anion Gap
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This is the difference between the measured
cations (Na+& K+) and the measured anions
(Chloride and Bicarbonate)
 Normally between 15-20Mmol/L
 Increases when unmeasured anions such as
phosphates and sulphates increase in the
blood and HCO3 falls in acidosis
 The converse occurs in metabolic alkalosis
METABOLIC DERANGEMENTS
Metabolic acidosis
 Respiratory acidosis
 Metabolic alkalosis
 Respiratory alkalosis
 Mixed picture (largely
compensational)
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Metabolic acidosis
This occurs when the primary
abnormality in the bicarbonate buffer
system is the reduction of (HCO3-).
Changes in pCO2 are secondary. When
(HCO3-) is reduced in the equation;
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pH = pK + log HCO3PCO2
 The pH will fall.
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Causes of Metabolic Acidosis
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Increased or excess H+ production:
Ketoacidosis, e.g., uncontrolled diabetes
mellitus, starvation, lactic acidosis, shock.
Poisoning, e.g., salicylate over-dosage,
 Failure to excrete H+: Acute and chronic
renal failure , distal renal tubular acidosis.
 Loss of HCO3- from GIT : Severe diarrhoea,
pancreatic fistula
 Loss of HCO3- in urine: Ureteroenterostomy, proximal renal tubular acidosis,
carbonic anhydrase inhibitors.
Compensation
Compensation for metabolic acidosis
occurs through the respiratory centre.
There is stimulation of the respiratory
centre resulting in hyperventilation to
’wash out’ CO2, and avoid a change in
pH.
 pH =6.1 + log (HCO3-)
PCO2x 0.23
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Renal Tubular Acidosis( RTA)
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Usually an acquired disorder
Could be inherited
No 10 glomerular lesion, urea & creatinine are
normal
Usually a tubular defect-2types
Classical or Type 1,Distal RTA-abnormal
permeability of distal tubular cells to H+
Proximal or type 2 -defect of Carbonic
anhydrase
Both result in metabolic acidosis
Respiratory Acidosis
This is characterized by an increase in
pCO2 due to CO2 retention.
 If pCO2 is increased in the equation:
pH = (HCO3-)
PCO2
pH will fall.
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Causes of Respiratory Acidosis
Pulmonary disease :Chronic
obstructive airway disease(COAD),
e.g, chronic bronchitis, emphysema,
severe asthma, pulmonary oedema.
 Chest infection: Bronchopneumonia
 CNS depression :Anaesthetics, opiates.
 CNS disease: Stroke, trauma.
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Compensation
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Compensation occurs by the
acceleration of the carbonic anhydrase
mechanism in the erythrocytes and renal
tubular cells, resulting in high HCO3
which could also lead to normal or no
change in pH.
Metabolic Alkalosis
This disorder is characterised primarily
by an increase in the concentration of
bicarbonate
 in the ECF, resulting in the reduction of
hydrogen ion concentration.
 When this occurs, bicarbonate
reabsorption is reduced, resulting in
bicarbonate excretion in urine.
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Causes of Metabolic Alkalosis
· Ingestion of large amount of
bicarbonate to treat indigestion.
 · Loss of unbuffered H+, e.g., Conn’s
and Cushing’s syndrome
 · Loss of H+ from GI tract vomiting,
e. g., nasogastric tube drainage pyloric
stenosis.
 · Loss of H+ in urine thiazide diuretics
Compenstion
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Largely by induction of respiratory
acidosis by CO2 retention to avoid a shift
in pH from the equation:
Respiratory Alkalosis
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This occurs when there is a fall in PCO2 which
reduces the ratio of pCO2 to bicarbonate
concentration in the pH equation.
 Causes are:
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Hysterical over breathing: Voluntary
hyperventilation, excessive artificial respiration
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Stimulation of Respiratory centre: Pain, fever,
hypoxia, Lobar pneumonia , Hypoxia, pulmonary
oedema
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Raised intracranial pressure or brain stem
lesions
Compensation
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There is a compensatory fall in the drive
of carbonic anhydrase system to reclaim
bicarbonate in both the kidneys and the
erythrocytes leading to a fall in HCO3- to
minimise the change in pH.
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