ACID- BASE

BALANCE
PRESENTER-DR. NYABWA
MODERATOR-DR C. NJERU
16/10/2024
DISCUSSION HEADINGS

► BASICS
► NORMAL PHYSIOLOGY
► ABNORMALITIES
► METABOLIC ACID BASE DISORDERS
► RESPIRATORY ACID BASE DISORDERS
► COMPLICATIONS
► ABGS
DEFINITION

► Acid-base disorders are pathologic changes in carbon

dioxide partial pressure (Pco2) or serum bicarbonate
(HCO3 −) that typically produce abnormal arterial pH
values.
► Acid
Any compound which forms H⁺ ions in solution (proton donors)
eg: Carbonic acid releases H⁺ ions

► Base
Any compound which combines with H⁺ ions in solution (proton
acceptors) eg:Bicarbonate(HCO3⁻) accepts H+ ions
❖ Normal pH : 7.35-7.45

❖ Acidosis
Physiological state resulting from abnormally low plasma
pH

❖ Alkalosis
Physiological state resulting from abnormally high plasma
pH
❖ Acidemia: plasma pH < 7.35

❖ Alkalemia: plasma pH > 7.45

Sources of Acids

⚫ 1. Respiratory (or volatile) acids: Carbonic

acid (H2CO3) derived from carbon dioxide
(CO2)
⚫ 2. Metabolic (or fixed) acids: Because they are
not excreted by the lungs they are said to be
‘fixed’ in the body. All acids other then H2CO3
are fixed acids. E.g. lactate, phosphate,
sulphate, acetoacetate or b-hydroxybutyrate.
Fixed acids are produced due to incomplete
metabolism of carbohydrates (eg lactate), fats
(eg ketones) and protein (eg sulphate,
phosphate).
 Henderson-Hasselbach
equation (clinically relevant
form)
-
► pH = pKa + log([HCO3 ]/.03xpCO2)

► pH = 6.1 + log([HCO3-]/.03xpCO2)

► Shows that pH is a function of the ratio

between bicarbonate and pCO2
► PCO₂ - ventilatory parameter (40 +/- 4)
► HCO₃⁻ - metabolic parameter (22-26 mmol/L)
Buffers

► It is a mixture of weak acid and its salt or weak base

and its salt, which resist pH change on addition of a
small amount of strong acid or alkali.
► The buffering capacity depends on actual
concentrations of salt and acid, and its ratio.
Examples
► Proteins- majority of intracellular buffering and a
portion of the extracellular fluid buffering.
► Phosphates- most important in buffering intracellular
fluid and urine.
► The bicarbonate-carbonic acid- most critical in
maintaining the pH of extracellular fluid.
9
Bicarbonate buffer system

The Carbonic Acid–Bicarbonate Buffer System

Phosphate buffer

► Major intracellular buffer

► H+ + HPO42- ↔ H2PO4-

11
 Protein Buffers

► Includes hemoglobin, proteins in ICF

+
► Carboxyl group gives up H
► Amino Group accepts H+
► Some Side chains of amino acid residues
can buffer H+ - lysine, arginine, histidine

12
Hemoglobin buffer system

► Histidine residue of hemoglobin can act as acid or base.

► Histidine amino acid has pKa value of 6.5 and it is
efficient buffer .
► Deoxygnatered hemoglobin in tissues accepts H+ ions to
form HHb. (KHb / HHb buffer )
► Oxygenated hemoglobin releases H+ ions in lungs.
► Amino groups of hemoglobin interact with CO2 to form
carbamino hemoglobin.
Renal regulation of pH

► Functions
► Reabsorption of bicarbonate involves the reabsorption
of bicarbonate filtered without excretion of H+ ions.
► Excretion of H+ ions
► Here there is net gain of bicarbonate for each H+
excretion. As the H+ ion excretion increases, the
excretion of H+ against concentration gradient becomes
difficult.
► So in the distal convoluted tubules, urinary buffers
buffer the free H+ ions.
Reabsorption of bicarbonate
Excretion of H+ ions
Urinary buffers

► Two important urinary buffers are

1. Phosphate buffer
2. Ammonia
► The maximum limit of acidification of urine is 4.5.
► Normally 70 meq acid is excreted daily. In metabolic
acidosis, this can raise to 400 meq/day.
Phosphate buffer
Ammonia buffer
COMPENSATION

► The body adapts, or compensates where there is an acid-base

disturbance in an attempt to maintain homeostasis.
► If the primary acid-base problem is metabolic, then the
compensatory mechanism is respiratory. The respiratory rate is
altered, usually within minutes, in an attempt to keep the
hydrogen ion concentration normal

► If the primary acid-base problem is respiratory, then the

kidneys adapt to counteract the change by altering their
handling of hydrogen ions. This process in the kidneys usually
takes place over several days.
Compensation cont.

► Hyper ventilation in metabolic acidosis reducing the

PaCO2 seen when there is an increase in H+
concentration in csf and detected by chemoreceptors
hence hyper ventilation to reduce CO2

► Hypoventilation in metabolic alkalosis increasing the

PaCO2
Primary Acid- Base Disorders

► Metabolic alkalosis
► Metabolic acidosis
► Respiratory alkalosis
► Respiratory acidosis
 Acid Base Disorders

Disorder pH [H+] Primary Secondary

disturbance response
Metabolic ↓ ↑ ↓ [HCO3-] ↓ pCO2
acidosis
Metabolic ↑ ↓ ↑ [HCO3-] ↑ pCO2
alkalosis
Respiratory ↓ ↑ ↑ pCO2 ↑ [HCO3-]
acidosis
Respiratory ↑ ↓ ↓ pCO2 ↓ [HCO3-]
alkalosis
Metabolic Acidosis

► Primary disorder
► ↓HCO₃⁻ → ↓ pH
► Gain of strong acid
► Loss of base(HCO₃⁻)
 ANION GAP CONCEPT
► To know if Metabolic Acidosis due to
✔ Loss of bicarbonate
✔ Accumulation of non-volatile acids
► [serum Na⁺ - (serum Cl⁻ + serum HCO₃⁻)]
► NORMAL RANGE= 8-12 mmol/L
► Mostly represent ALBUMIN
Anion gap metabolic acidosis
(AGMA) >12
Non-anion gap metabolic
acidosis(NAGMA) <12
Causes
► Hyperchloridemia
► Acetazolamide
► Renal tubular acidosis
► Diarrhea
► Urethral diversion
► Pancreatic fistula
Used to asses elevated anion gap metabolic acidosis and to
determine whether there is a mixed acid-base disorder

delta ratio= measured anion gap -12 / 24 - measured

HCO3

❖ 12 being normal anion gap

❖ 24 normal HCO3-
DELTA GAP INT

► If gap-gap = 1-2 - this represents a pure high AG

metabolic acidosis.
► If gap-gap > 2, there is both a high AG metabolic
acidosis and an added metabolic alkalosis.
► If gap-gap < 1, there is both high AG metabolic
acidosis and an added normal AG metabolic acidosis.
 Compensation for Metabolic
acidosis
► Hyperventilation – to reduce PCO₂
► ↓pH sensed by central and peripheral chemoreceptors
► ↑ in ventilation starts within minutes,well advanced at 2 hours
► Maximal compensation takes 12 – 24 hours
Metabolic Alkalosis

► ↑ pH due to ↑HCO₃⁻ or ↓acid

 CAUSES OF METABOLIC ALKALOSIS
I. Exogenous HCO3 − loads
A. Acute alkali administration
B. Milk-alkali syndrome

II. Gastrointestinal origin

1. Vomiting
2. Gastric aspiration
3. Congenital chloridorrhea
4. Villous adenoma

III. Renal origin

1. Diuretics
2. Posthypercapnic state
3. Hypercalcemia/hypoparathyroidism
4. Recovery from lactic acidosis or ketoacidosis
5. Nonreabsorbable anions including penicillin, carbenicillin
6. Mg2+ deficiency
7. K+ depletion
 Compensation for Metabolic
►
Alkalosis
Respiratory compensation: HYPOVENTILATION
❖ ↑PCO₂
Respiratory Acidosis

► ↑ PCO₂ → ↓pH
► Acute(< 24 hours)
► Chronic(>24 hours)
causes

► Central nervous system depression.

► Respiratory muscle weakness,
paralysis, or chest wall constriction
► Airway obstruction e.g COPD
► Overproduction of CO2- thyroid
storm, malignant hyperthermia, or
early sepsis.
► Iatrogenic- Mechanical Ventilation
 Compensation in Respiratory Acidosis
❖ HCO₃⁻ ↑
✔ Maximal response : 3 - 4 days
Respiratory Alkalosis

► Most common AB abnormality in critically ill

► ↓PCO₂ → ↑pH
► 1⁰ process : hyperventilation
► Acute: PaCO₂ ↓,pH-alkalemic
► Chronic: PaCO₂↓,pH normal / near normal
 CAUSES OF RESPIRATORY ALKALOSIS
C. Drugs or hormones
A. Central nervous 1. Pregnancy, progesterone
system stimulation 2. Salicylates
1. Pain 3. Cardiac failure
2. Anxiety, psychosis D. Stimulation of chest receptors
3. Fever
1. Hemothorax
4. Cerebrovascular accident
2. Flail chest
5. Meningitis, encephalitis
3. Cardiac failure
6. Tumor
4. Pulmonary embolism
7. Trauma
E. Miscellaneous
B. Hypoxemia or 1. Septicemia
tissue hypoxia 2. Hepatic failure
1. High altitude 3. Mechanical ventilation
2. Septicemia 4. Heat exposure
3. Hypotension 5. Recovery from metabolic
4. Severe anemia acidosis
 Compensation for respiratory
✔ Renal compensation (acid retention,HCO₃⁻ loss)
✔
Alkalosis
Starts after 6 hours, maximal response 2- 3 days
Mixed Acid- Base Disorders

► PCO2 and HCO3- concentrations change in opposite

directions
► pH is normal, but PCO2 or HCO3- is abnormal
► The compensation is significantly different from
expected
► Respiratory acidosis and alkalosis never coexist
► Metabolic disorders can coexist
COMPLICATIONS
heart acidosis alkalosis

CO/MAP decrease normal

TPR decrease Increase

HR increase increase
Metabolic and acidosis alkalosis
lung

potassium hyperkalemia hypokalemia

magnesium normal hypomagnesia

calcium normal hypocalcemia

RR increased Reduced
ACID-BASE DISORDERS – A FOUR(+1) STEP
APPROACH

► In order to understand the nature of an acid-base problem, a

structured approach during which the following four(five)
questions should be asked ,what is?

1. PH
2. Bicarbonate
3. PCO2
4. Anion gap
5. Delta ratio
examples

► Ph 7.44, pco2-56, hco3 of 37

► Ph 7.29, pco2 58, hco3 of 22
► Ph 7.32, pco2 34, hco3 of 14
► Ph 7.25, pco2-25, hco3 of 10
THE END