ACID BASE DIORDER

• DR GAZI SABIR ULLAH

• DR KANIZ AKTER KRISTY
 Normal ABG values
pH 7.35-7.45
pCO3 35-45 mmHg
pO2 50-70 mmHg
HCO3 20-28 mEq/L
BE ±5
Terminology used in acid base disorders
• Proton(H⁺): Proton is the hydrogen atom with its
electron removed.
• Acid: An acid is a substance that release a hydrogen
ion.
• Base: A base is a substance that accepts a hydrogen
ion.
• Akali: Alkali is metallic hydroxide which in solution
ionizes to hydroxyl ion(OH⁻) that can accept the
proton from solution forming water.
e.g. NaOH,KOH etc.
• Conjugate base of an acid: It is the remaining part of an acid after
donation of proton.
e.g. Cl⁻(conjugate base of HCl), HCO₃⁻(conjugate base of H₂CO₃).
• Congugate acid of base: It is the acid formed by a base after
accepting proton.
e.g. HCl is the conjugate acid of chloride(Cl⁻).
• pH: It is the negative logarithm of hydrogen ion concentration of a
solution, when concentration expressed in terms of molarity
(mol/L).
pH: - log[H⁺].
• Buffer: Buffers are substances that attenuate the change in pH that
occurs when acids or bases are added to the body.
• Acidemia: An arterial pH below the normal
range (less than 7.35).
• Alkalemia: An arterial pH above the normal
range (greater than 7.35).
• Hypoxia: When pO₂<50 mmHg.
• Hyperoxia: When pO₂>70 mm Hg.
• Acidosis: A process that tends to lower the
extracellular fluid pH (hydrogen ion
concentration increases).
• Alkalosis: A process that tends to raise the
extracellular fluid pH (hydrogen ion
concentration decreases).
 Importance of normal body pH
• Supports optimum enzyme activity for smooth running of
metabolism.
• Maintains the native molecular form and structural
conformation of biomolecules(specially proteins) at which they
are functionally active.
• Maintains internal environment and cellular viability by turning
proper electrolyte distribution in ECF through Na⁺-K⁺ pump.
• Maintains optimum vascular resistance.
• Concerned with oxygen-hemoglobin dissociation and
association realtionship.
• Concerned with chemical control of respiration.
Routes of acid excretion from body
• Pulmonary route: It is the route for excretion
of volatile acid only.
e.g. CO₂ or H₂CO₃
• Renal route: It is the route for excretion of
both nonvolatile acid and base.
e.g. nonvolatile acid or fixed acid(HCl, H₂SO₄,
H₃PO₄, lactic acid, ketoacid etc.)
 Defense of pH
First line defense:
 Body buffer system (its acts within second to
minutes).
 Pulmonary system(it acts within minutes to
hours by regulating CO₂ content).
Second line defense:
 Renal system(it acts within hours to days by
regulating serum bicarbonate and excretion of
acid0.
 Distribution of body buffers
Compartment Buffers
Blood Bicarbonate, hemoglobin, phosphate,
protein.
RBC hemoglobin, phosphate, bicarbonate
ECF Bicarbonate, phosphate, protein
ICF Protein, bicarbonate, phosphate.
Urine Ammonia, phosphate, bicarbonate
 Buffers and Henderson-Hasselbalch
equation
• All buffers are related to body pH by the
principle of Henderson-Hasselbalch equation
as given below : pH= pK+log Base/Acid
 Bicarbonate buffer
• The bicarbonate buffer system is routinely monitored clinically
and is based on the relationship between carbon dioxide(CO₂)
and bicarbonate(HCO₃⁻):
CO₂+H₂O ↔ H⁺ + HCO₃⁻
• The Henderson-Hasselbalch equation for bicarbonate(HCO₃⁻)
and carbon dioxide(CO₂) is as follows: pH= 6.1+ log[HCO₃⁻]/[CO₂]
=6.1+ log
[24mmol/L]/[1.2mmol/L]
= 6.1+ log 20
=6.1+1.3
=7.4
• Maintain a 20:1 ratio: HCO₃⁻: H₂CO₃
• The bicarbonate buffer system is an open
system because the lungs increase CO2
excretion when the blood CO2 concentration
increases. When acid is added to the body, the
following reaction occurs:
CO₂+H₂O →H⁺ + HCO₃⁻
 Phosphate buffer
• Major intracellular buffer.
• H⁺+HPO₄²⁻ ↔ H₂PO₄⁻
• OH⁻+ H₂PO₄⁻ ↔H₂O+ H₂PO₄²⁻
• Although phosphate is an effective buffer, its
buffering capacity is limited by its
concentration; there is no mechanism for
increasing urinary phosphate excretion in
response to changes in acid-base status
 Protein buffer
• Major intracellular buffer.
• Proteins are effective buffers, largely because
of the presence of the amino acid histidine,
which has a side chain that can bind or release
H⁺.
• Carboxyl group gives up H⁺.
• Amino group accepts H⁺.
 Hemoglobin buffer system
• Histidine residue of hemoglobin can act as acid
or base.
• Histidine has pKa value of 6.5 and its is efficient
buffer.
• Deoxyhemoglobin in tissues accepts H⁺ ions to
form HHb.(KHb/HHb buffer)
• Oxygenated hemoglobin release H⁺ ions in lungs.
• Amino groups of hemoglobin interact with CO₂
to form carbamino hemoglobin.
• Action of hemoglobin buffer:
In tissues, CO₂ diffuses into erythrocytes to
form carbonic acid by carbonic anhydrase.
H₂O + CO₂ ↔ H₂CO₃
H₂CO₃ ↔ H⁺ + HCO₃⁻
KHb accepts H⁺ and release K⁺.
Bicarbonate diffuses into plasma where is
concentration low.
• In lungs, oxygenation of hemoglobin release
H⁺ which combines with bicarbonate to form
carbonic acid by carbonic anhydrase.
 Carbonic acid dissociates into water and CO₂.
 CO₂ is expired out by lungs.
 Chloride comes out in exchange for HCO₃⁻ to
maintain electrical neutrality.
 Renal regulation of pH
• The kidneys regulate the serum bicarbonate
concentration by modifying acid excretion in
the urine. This requires a 2-step process.
 First, the renal tubules resorb the bicarbonate
that is filtered at the glomerulus.
 Second, there is tubular secretion of H+ . The
urinary excretion of H+ generates bicarbonate
that neutralizes endogenous acid production.
 Urinary buffers
• Two important urinary buffers are
1) Phosphate buffer
2) Ammonia.
 Bone buffer
• Chemically bone buffer is the alkaline calcium- phosphate salt of
bone deposited in the form of hydroxyapatite crystal(HAC).
• During mineralization of bone, calcium and phosphate is
deposited in the form of HAC with release of H⁺ and the process
is reversible.
Cₐ₉(PO₄)₆ + Cₐ⁺⁺ + 2H₂O↔ Cₐ₁₀(PO₄)₆(OH)₂ + 2H⁺
• During persistent acidosis, high plasma proton concentration
shifts the equilibrium of the reaction towards the left and HAC
takes up H⁺ to reverse the process of mineralization ar the cost
of dissolution of HAC leading to osteoporosis change in bone.
Therefore, calcium releases from bone to cause hypercalcemia
and calciuria.
ACID BASE IMBALANCE
 ABD & Respective compensations and corrections
ABD Primary Compensations Corrections
Disturbance
Metabolic acidosis p[HCO3]a Paco2 by Renal excretion of
hyperventilation acid

Metabolic alkalosis p[HCO3]a Paco2 by Renal excretion of

hypoventilation base

Respiratory acidosis paco2 p[HCO3]a Pulmonary

excreation of co2
Transient excreation
of acid and
reabsorption of
base

Respiratory acidosis paco2 p[HCO3]a Pulmonary

retention of co2
Transient
suppression of acid
and excretion of
base
ABD Formulas of Limits
predication

Metabolic Paco2=(1.5*HCO3) 10 mm Hg
acidosis 8±2

Matabolic Paco2=(0.9*HCO3) 55 mm Hg
alkalosis 9±2

Respiratory HCO3=PACO2*0.4 18 mEq/liter

acidosis

Respiratory HCO3=PACO2*0.25 30 mEq/liter

alkalosis
 Compensation

• If underlying problem is metabolic hyperventilation

or hypoventilation can help respiratory
compensation.

• If problem is respiratory renal mechanism bring out

metabolic compensation
 Metabolic acidosis

Metabolic acidosis is characterized by a reduction in

serum bicarbonate and a consequent rise in H+ .

• Mechanism of metabolic acidosis

1. Loss of bicarbonate from body

2. 2. Excess acid production in body
3. 3. Impaired ability to excrete acid by kidney
 Causes of metabolic acidosis

Normal Anion Gap:

1.Diarroea
2. Proximal renal tubular acidosis
3. Distal renal tubular acidosis
4. Hyperkalemic renal tubular acidosis
5. Ammonium chloride intake
Increased Anion Gap :

1.Tissue hypoxemia
2. Shock
3. Hypoxemia
4. Severe anemia
5. Liver failure
6. Intestinal bacterial growth
7. Medication such as
Metformin, propofol Linezolid
etc
8. Ketoacidosis such as diabetic
ketoacidosis, starvation ketoacidosis
Alcoholic acidosis.
9. Poisoning by salicylate, ethylene glycol,
methanol etc.
10. Renal failure.
Symptoms of metabolic acidosis

• Persistent hyperventilation
• vomiting
• kussmaul breathing
• lethargy
• unconsciousness
• convulsion
• Hypertonia
• Ventricular dysrhythmia
• impairment of myocardial
contractility
 Treatment

Most often therapeutic approach for the patient with

metabolic acidosis is repair undying cause.Such as
administration of insulin in DKA and the restoration
of adequate perfusion with intravenous fluid.Children
with metabolic acidosis cause by RTA required long
time base therapy.In salicylate poisoning alkali
administration increase renal clearance.Iv or oral
base therapy can be used in acute metabolic
acidosis .
Intravenous route is generally used when a rapid
response is required.Sodium bicarbonate may be given
as a bolus usually as a dose of 1 mEq/kg.The risk of
giving sodium bicarbonate include the possibility of
causing hypernatremia, volume overload, cardiac
arrhythmia etc.Hemodialysis is other option for
correcting metabolic acidosis and it is an appropriate
choice for the patient with renal insufficiency. specially
if significant hyperkalemia or uremia present.Peritoneal
dialysis is another option for patient with chronic kidney
disease.
 Metabolic Alkalosis

Metabolic Alkalosis in manifested by an elevation of

arterial Ph ,an increase in serum HCO3 and an increase
in serum paCo2 as a result of compensatory
hypoventilation.
 Mechanism of metabolic Alkalosis

The etiology of metabolic Alkalosis dividend into 2

categories Based of urinary chloride level.Alkalosis in
patient with low urinary chloride level is maintained by
volume depletion.It is caused by losses of sodium and
potassium but the loss of chloride is usually greater
than loss of sodium and potassium combined.They are
said to have chloride responsive metabolic Alkalosis In
contrast the alkalosis in a patient with elevated urinary
chloride does not respond to volume replation so is
termed chloride resistant metabolic Alkalosis
 Causes of metabolic Alkalosis

1. Chloride responsive metabolic Alkalosis

Vomiting
Naso-gastric suction
Cystic fibrosis
Diuretics: thaizide or loop
2. Chloride resistant metabolic Alkalosis
A. High blood pressure
Adrenal hyperplasia or adenoma
Familial hyperaldosteronism
Renin secreting tumor
Renovascular disease.
Liddle syndrome
Cushing syndrome
Normal blood pressure
Bartter syndrome
EAST syndrome
Autosomal dominant
hypoparathyroidism
Hyperuricemia
Clinical manifestation of
metabolic Alkalosis

• neurological dysfunction
• muscle weakness
• muscle twitching
• tetany,
• cardiac arrhythmia
 Treatment

The approach to treatment of metabolic Alkalosis

Depends on the severity of alkalosis And the
underlying etiology In case of mild alkalosis
Intervention is often unnecessary although it's
depends on special circumstances.In a child with
congenital heart disease Who receive a stable
dose of loop diuretics a mild alkalosis don't
require Adequate potassium supplimentation or
the addition of potassium sparing diuretics is also
helpful in a child with a metabolic Alkalosis from
diuretics.
Potassium sparing diuretics not only decrease renal
potassium losses they also block the action of
aldosterone also decrease hydrogen ion secretion in
the distal nephron and increase urinary bicarbonate
excretion.In severe alkalosis acetazolamide inhibitor is
an option it decrease resorption of bicarbonate in
proximal renal tubule causing significant bicarbonate
loss in urine .In children with chloride resistant
metabolic Alkalosis Treatment focus on eliminating the
excess aldosterone effect.
 Respiratory Acidosis
Respiratory Acidosis is characterized by an
increase in paCO2 and decrease in PH.

Mechanism of respiratory acidosis

• By depressing the respiratory system
• In lung though intrinsic disease
• Respiratory muscle weakness.
 Causes of respiratory Acidosis

CENTRAL NERVOUS SYSTEM DEPRESSION

• Encephalitis
• Head trauma
• Central sleep apnea
• Primary pulmonary hypoventilation (Ondine curse)
• Stroke
• Hypoxic brain damage
• Obesity
• hypoventilation
• (Pickwickian) syndrome
• increased intracranial pressure
• Medications
• Narcotics
• Barbiturates
• Anesthesia
DISORDERS OF SPINAL CORD, PERIPHERAL NERVES,
OR NEUROMUSCULAR JUNCTION

• Diaphragmatic paralysis
• Guillain-Barré syndrome
• Poliomyelitis
• Acute flaccid myelitis
• Spinal muscular atrophies
• Tick paralysis
• Botulism
• Myasthenia
• Multiple sclerosis
• Spinal cord injury
• Medications
• RESPIRATORY MUSCLE
• Weakness
• Muscular dystrophy
• Hypothyroidsm
• Malnutrition
• Hypokalemia
• Hypophosphatemia
• Medications
Succinylcholine
Corticosteroide
PULMONARY DISEASE
• Pneumonia
• Pneumothorax
• Asthma
• Bronchiolitis
• Pulmonary edema
• Pulmonary hemorrhage
• Acute respiratory distress syndrome
• Neonatal respiratory distress syndrome
• Cystic fibrosis
• Bronchopulmonary dysplasia
• Hypoplastic lungs
• Pulmonary thromboembolus
• Interstitinl fibrosis
UPPER AIRWAY DISEASE

• Aspiration
• Laryngospasm
• Angioedema
• Obstructive sleep apnea
• Tonsillar hypertrophy
• Vocal cord paralysis
• Extrinsic tumor
• Extrinsic or intrinsic hemangioma
 manifestation of
Respiratory acidosis

1. Hypoxemia cause cerebral

vasodilation
2. Papilloedema by
increased intracranial
pressure
3. Headache
4. Drowsiness.
 Treatment

Respiratory acidosis is best managed by treatment of the

underlying etiology. In some patients, the response is
very rapid, such as after the administration of naloxone
to a patient with a narcotic overdose. In contrast, in the
child with pneumonia, a number of days of antibiotic
therapy may be required before the respiratory status
improves. In many children with a chronic respiratory aci-
dosis, there is no curative therapy, although an acute
respiratory illness superimposed on a chronic respiratory
condition is usually reversible. All patients with an acute
respiratory acidosis are hypoxic and therefore need to
receive supplemental oxygen. Mechanical ventilation is
necessary in some children with respiratory acidosis.
Children with significant respiratory acidosis caused by CNS
disease usually require mechanical ventilation because such a
disorder is unlikely to respond quickly to therapy. In addition,
hypercarbia causes cerebral vasodilation, and the increase in
ICP can be dangerous in a child with an underlying CNS
disease. Readily reversible CNS depression, as from a narcotic
overdose, may not require mechanical ventilation.Decisions
on mechanical ventilation for other patients depend on a
number of factors. Patients with severe hypercarbia (Pco, >75
mm Hg) usually require mechanical ventilation (see Chapter
86.1). The threshold for intubation is lower if there is
concomitant metabolic acidosis, a slowly responsive
underlying disease, or hypoxia that responds poorly to
oxygen, or if the patient appears to be tiring and respiratory
arrest seems likely.
 Respiratory Alkalosis

Respiratory Alkalosis results from a primary

increase of ventilation with subsequent fall in
plasma pCO2 and rised plasma PH.
 Causes of respiratory Alkalosis

• HYPOXEMIA OR TISSUE HYPOXIA

1. Pneumonia
2. Pulmonary edema
3. Cyanotic heart disease
4. Congestive heart failure
5. AsthmaSevere anemia
6. High Altitude
7. Laryngospasm
8. Aspiration
9. Carbon monoxide poisoning
10. Pulmonary embolism
11. Interstitial lung disease
12. Hypotension
• LUNG RECEPTOR STIMULATION
1. Pneumonia
2. Pulmonary edema
3. Asthma
4. Pulmonary embolism
5. Hemothorax
6. Pneumothorax
7. Respiratory distress syndrome (adult or
infant)
• CENTRAL STIMULATION
1. Central nervous system disease
2. Subarachnoid hemorrhage
3. Encephalitis or meningitis
4. Trauma
5. Brain tumor
6. Stroke
7. Fever
8. Pain
9. Anxiety (panic attack)
10. Psychogenic hyperventilation
11. Liver failure
12. Sepsis
13. Pregnancy
14. Mechanical ventilation
• Hyperammonemia
• Extracorporeal
membrane oxygenation
or hemodialysis
• Medications
• Salicylate intoxication
• Theophylline
• Progesterone
• Exogenous
catecholamines
• Caffeine
Clinical manifestation of Respiratory Alkalosis
1. Paraesthesia
2. Muscle twitching
3. Alter mental status
4. Convulsion
 Treatment of respiratory Alkalosis

There is seldom a need for specific treatment of

respiratory alkalosis.Rather, treatment focuses on the
underlying disease. Mechanical ventilator settings are
adjusted to correct iatrogenic respiratory alkalosis, unless
the hyperventilation has a therapeutic purpose (e.g.,
treatment of increased ICP).For the patient with
hyperventilation secondary to anxiety, efforts should be
undertaken to reassure the child, usually enlisting the
par-ents. Along with reassurance, patients with
psychogenic hyperventilation may benefit from
benzodiazepines.
During an acute episode of psychogenic hyperventilation,
rebreathing into a paper bag increases the patient's Pcoz.
Using a paper bag instead of a plastic bag allows adequate
oxygenation but permits [COz] in the bag to increase. The
resultant increase in the patient's Pco, decreases the
symptoms of the respiratory alkalosis that tend to
perpetuate the hyperventilation.Rebreathing should be
performed only when other causes of hyperventilation
have been eliminated; pulse oximetry during the
rebreathing is prudent.