ACID BASE DISORDERS
Dr. Hayam Hebah
Associate professor of Internal Medicine
AL Maarefa College
Definitions
• Acid (HA) is defined as a compound that can release
a proton (H+)
• Normal pH = 7.35 – 7.45
• Acidosis (acidaemia) is defined as a disorder with
accumulation of acids .The pH is < 7.35
• Base (B-) can bind H+
• Alkalosis (alkalaemia) is defined as a condition with
accumulation of bases . The pH is › 7.45
• Buffer is a mixture of compounds which have the
ability to absorb small amounts of H+ or OH- with very
little change of pH.
• pH: it is a measure of H + activity
Production of acids
• Volatile acids:
● CO2 is a potential acid as H2CO3, and because the lungs eliminate it, it is
called a volatile acid. Production of CO2 is up to 24 mol daily.
● Non-volatile acids:
a) organic acids are continually produced as a by-product of metabolism:
- anaerobic glycolysis in muscles → lactic acid → lactate + H+
- ketogenesis → acetoacetic acid → acetoacetate + H+
→ β-hydroxybutyric acid → β-hydroxybutyrate + H+
- lipolysis → TAG → 3 FA + glycerol + 3 H+
- urea synthesis in liver: CO2 + 2 NH4 → urea + H2O + 2 H+
Under normal conditions, these acids are completely metabolized to CO2 and
H2O. They have no effect on proton balance.
b) inorganic acids: excretion by kidneys
H2SO4 → HSO4- + H+
H3PO4 → HPO42- + H+
Note: H+ are also released from acids in the diet
e. g. citric acid, ascorbic acid
The body maintains ECF physiologic pH by
buffers
•
•
•
•
Bicarbonate buffer HCO3- / CO2
Hemoglobin (Hb)
Plasma proteins (mainly albumin)
Phosphate buffer HPO42- / H2PO4-
(53%)
(35%)
(7%)
(3%)
NH3/NH4+ and HPO42-/H2PO4- are the most important
urinary buffer systems.
Mechanisms for the Homeostasis of
Hydrogen Ions
• Despite the continual metabolic production of acid, the pH of ECF is
normally tightly maintained between 7.35-7.45.
• The primary organs that deal with the acid load are:
the lung (respiratory) and kidneys (metabolic).
• Kidney (24-48h) The kidneys maintain the bicarbonate buffer system.
They do this by retaining existing bicarbonate and generating new
bicarbonate to replace that destroyed by the buffering of nonvolatile acids
• Lungs ( rapid within 1-3 minutes) Eliminate carbon dioxide, maintaining a
concentration of CO2 in the body fluids.
↑ ventilation → ↓ pCO2 → alkalinization
↓ ventilation → ↑ pCO2 → acidification
•
Chemical buffer within seconds 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 ions.
HCO3- elimination is controlled by kidneys. It takes several hours
to days for urinary system to compensate for changes in pH.
Liver: CO2 + 2 NH4 → urea + 2 H+ + H2O
NH4+ + Glu → Gln + H2O
Laboratory analysis of ABB state
• Determination of pH, HCO3-, pCO2, pO2 and BE
• Determination of concentration of cations (Na+, K+,
Ca2+, Mg2+), concentration of anions (Cl-, lactate) and
metabolites (urea, creatinine, ketone bodies)
Normal values of:
• HCO3- = 22 – 26 mmol/L
• BE = from – 2.5 to + 2.5 mmol/L
BE (base excess) is defined as the amount of acid that
would be added to blood to titrate it to pH 7.4 at pCO2
= 40 mmHg.
positive value = base excess
negative value = base deficit (BD)
Anion gap (AG)
AG represents the plasma anions which are not routinely
measured (albumin, phosphates, sulphates, organic
anions).
AG is calculated as follows:
AG = (Na+ + K+) – (HCO3- + Cl-)
AG= Na+ -HCO3- + Cl-)
The sum of the concentrations of Na+ and K+ is greater
than the sum of concentrations of HCO3- and Cl-.
Difference is called as a anion gap.
Normal values of AG: 16 – 20 mmol/L
AG is calculated in case of metabolic acidosis.
Metabolic acidosis
caused by accumulation of acids in ECF.
● negative BE
●
Causes:
• hypoxia is a lack of O2 in tissues → anaerobic glycolysis
produces lactic acid → lactate acidosis
• overproduction of ketone bodies → ketoacidosis (DM,
starvation)
• ingestion of methanol or ethylene glycol
• diarrhoea
Compensation:
1st step: buffering of excess of H+ by HCO32nd step: respiratory compensation by hyperventilation
3rd step: renal correction → ↑ excretion of H+ in urine
METABOLIC ACIDOSIS
NORMAL ANION GAP
(HYPERCHLOREMIC) 8-12 mEq
HIGH ANION GAP
>12 mEq
•
•
-
• Metabolic anion:
-DKA
-Alcoholic ketoacidosis.
-Lactic acidosis
-Renal failure
-starvation
• Drugs:
-salicylates
-methanol.
-Ethylene glycol
-carbenicillin treatment.
Loss of bicarbonate:
Diarrhea
Pancreatic fluid loss
Ileostomy
Carbonic anhydrase inhibitors
Chloride retention:
Renal tubular acidosis.
Ileal loop bladder
TPN
Treatment of metabolic acidosis:
1. Ttt of the cause :
e.g: ttt of DKA, diarrhea, stop PF.
2-Bicarbonate if PH<7.1
3- water replacement and correction of
electrolytes.
4- dialysis is necessary for severe metabolic acidosis
( as in renal failure cases)
HCO3(mEq)=0.5*wt(kg)*(24-serum HCO3)
Vials are 8.4%(10 mEq/10 mL).
Metabolic alkalosis(MAl)
•
•
caused by a primary accumulation of bases in ECF.
the BE is increased: Both the [bicarbonate] and the [non-carbonic buffer
base] are increased
Causes:
• ingestion of alkaline drugs (e. g. NaHCO3), MILK ALKALI SYNDROME
• prolonged vomiting → loss of H+.
•
gastric
juice loss by suction
•Mineralocorticoid (renal acid excretion)
•diuretic use(chloride loss in urine) .
Compensation:
1st step: buffering of excess of HCO32nd step: respiratory compensation by hypoventilation → ↑ pCO2 in alveoli and
arterial blood
3rd step: renal correction: ↑ excretion of HCO3- in urine
treatment:
• Restoration of normal body water volume, k,
cl and Na
• The anion given should be chloride until
correction is achieved (Nacl).
Respiratory acidosis (RAc)
RAc is caused by hypoventilation . Hypoventilation is associated
with an impaired ability to eliminate CO2, whereby pCO2
increases and the accumulated CO2 reduces the arterial pH.
Causes:
1. airway obstruction: COPD , Emphysema
2. neuromuscular disorders: kyphoscoliosis, respiratory muscle
weakness or paralysis
3. disorders of CNS depressing the respiratory centre :.
---opiate poisoning
-----Anesthesia.
Compensation: ↑ reabsorption of HCO3- is performed by kidneys
(proximal tubule)
Treatment:
1. Improve ventilation by maintaining open airway,
use mechanical aid, bronchodilators.
2. Ttt of hypoxia by oxygen therapy
3. Endotracheal intubation
4. Noninvasive positive pressure ventilation
N.B:IN cases with hypercapnia, oxygen therapy for
hypoxemia may deprive the patient of the only
remaining stimulus of the respiratory center and
may produce more hypoventilation and co2
narcosis.
Respiratory alkalosis (RAl)
The hyperventilation is disproportionately high compared to
the CO2 production, whereby the pCO2 falls and the pH
increases
Causes:
1. CNS injury
2. salicylate poisoning
3. fever, …
4. Other typical cases are the anxious patient during an
attack of asthma or the hysterical hyperventilation in
neurotic patients.
Compensation: ↑ renal excretion of HCO3- → plasma pH
decreases toward normal pH
Treatment:
• Reduce anxiety by anxiolytics or
psychotherapy.
• Tetany may be relieved by rebreathing
exhaled air which will increase PCO2 and
lower blood PH.
Renal Tubular Acidosis
• Renal tubular acidosis (RTA) is applied to a
group of transport defects in the reabsorption
of bicarbonate (HCO3-), the excretion of
hydrogen ion (H+), or both.
• The RTA syndromes characterized by:
Relatively normal GFR .
• Hyperchloremia Metabolic Acidosis (with
normal plasma anion gap).
Characteristics of types 1,2,4 RTA
Type 1
Type 2
Type 4
Primary defect
defect in distal
Decreased proximal
hydrogen ion
HCO3 reabsorption
excretion I e Impaired
urine acidification
Aldosterone def. or
resistance
Urine PH
>5.3
Variable >5.3 if HCO3
> reaborbed
threshold and < 5.3 if
below
Plasma HCO3
May be < 10meq/L
Above 12meq/L
Above 17meq/L
Plasma K
Usually reduced
rarely elevated
Normal or reduced
worsen by alkali
elevated
≥5.3
Type 1
Type 2
Type 4
Diagnosis
Response to
NaHCO3 or
ammonium
chloride
Response to
NaHCO3
Measurement of
plasma aldosterone
Therapeutic
amount of NaHCO3
required
1-3 meq/kg/d
10-15 meq/kg/d
1-3 meq/kg/d
Non-electrolyte
complications
Nephrocalcinosis
and renal stones;
Osteomalacia
uncommon
Rickets in children
and Osteomalacia
in adults; calculi is
rare.
None
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