This document provides an overview of acid-base physiology, including:
- Definitions of acids, bases, and acid-base balance
- The three main systems that maintain pH balance: buffers, respiration, and renal
- The four basic types of acid-base imbalances: metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis
- Details on specific disorders like respiratory acidosis, metabolic acidosis, and mixed disorders
- Compensatory responses and interpretation of blood gas measurements
- Case studies on mixed disorders involving respiratory and metabolic components
In under 3 sentences, it summarizes key concepts in acid-base physiology and provides examples of interpreting acid-base imbalances.
3. ACID AND BASE
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
Acids and bases can be Strong or Weak
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4. ACID–BASE BALANCE
Normal pH : 7.35-7.45
Homeostasis of pH is tightly controlled
Extracellular fluid = 7.4
Blood = 7.35 – 7.45
< 6.8 or > 8.0 death occurs
If any of these changes causes the pH to change to a value
outside the normal range, the suffix emia is used to describe
the acid-base derangement:
Acidosis (acidemia) below 7.35
Alkalosis (alkalemia) above 7.45
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5. 3 SYSTEMS THAT MAINTENANCE PH
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• Moves or release hydrogen ions
1. Buffers
• Regulate carbonic acid by eliminating or retaining
CO2
2. Respiratory system
• Long term regulation of acid-base in body by
regulating bicarbonate ions.
3. Renal system
6. 1. BUFFER SYSTEMS
Chemical buffers are available in extracellular/ intracellular
compartments
• Phosphate
• Protiens
• bicarbonate
Helps to maintain a stable pH , Removes or release H+
ions
• Excess acid (acidosis) pH <7.35, buffers bind with H+
ions
• Too alkaline (alkalosis) pH >7.45, buffers release H+
ions
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7. Bicarbonate system constituted of plasma sodium
bicarbonate (NaHCO3) and carbonic acid (H2CO3) and
cellular H2CO3 and potassium bicarbonate (KHCO3)
extracellular space
The phosphate system found in renal tubular fluid and
intracellularly
Proteins intracellular spaceMostl powerfull in
Most dominating in
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Three buffering systems
8. 2. RESPIRATORY SYSTEM
Normal PaCO2 = 35- 45 mmHg
Pulmonary buffering system is as effective as the chemical
buffering system . The lungs respond to deviations in pH by
altering the rate and depth of ventilation. Eliminates or retains
carbon dioxide
↑ carbon dioxide (acid) stimulate respiration
↑rate & depth of resp ↓ pH to normal range
Alkalosis depresses respiration
↓ rate & depth of resp retains carbon dioxide
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9. The kidneys are the third line of defence against wide
changes in body fluid pH
• movement of bicarbonate
• Retention/Excretion of acids
• Generating additional buffers
Long term regulator of ACID – BASE balance
May take hours to days for correction
3. Renal System
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10. Role of kidneys is
preservation of body’s
bicarbonate stores
• by controlling
serum bicarbonate
concentration
through the
regulation of H+
excretion
• bicarbonate
reabsorption
• production of new
bicarbonate
Proximal
tubule: 70-
90%
Loop of Henle:
10-20%
Distal tubule
and collecting
ducts: 4-7%
RENAL
REABSORPTION
OF BICARBONATE
i. MAINTAIN BICARBONATE
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11. Regeneration of titrated bicarbonate by
excretion of:
• Titratable acidity (mainly phosphate)
• Ammonium salts
ii. Regeneration Of Bicorbonate
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12. • TITRATABLE ACIDITY
Occurs when secreted H+
encounter & titrate phosphate
in tubular fluid
Refers to amount of strong
base needed to titrate urine
back to pH 7.4
40% (15-30 mEq) of daily
fixed acid load
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13. • AMMONIUM EXCRETION
Occurs when secreted H+
combine with NH3 and are
trapped as NH4
+ salts in tubular
fluid
60% (25-50 mEq) of daily fixed
acid load
Very adaptable (via
glutaminaseinduction)When
blood acidity is significantly
increased, glutamine
metabolized into ammonia.
Ammonia→ recipient of H+.
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14. Normal bicarbonate 22-26 mEq/L
Acidosis
• Excess H+ ions
• pH falls
• kidneys excrete H+ and retain bicarbonate
Alkalosis
• Less H+ ions
• pH increases
• Kidneys retains H+ ions & excrete bicarbonate
Interactions Among The Carbonic Acid–
bicarbonate Buffer System And Compensatory
Mechanisms In The Regulation Of Plasma pH
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15. Interactions among the Carbonic Acid–Bicarbonate Buffer System
and Compensatory Mechanisms in the Regulation of Plasma pH
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16. HENDERSON-HASSELBACH EQUATION
pH = pKa + 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)
3
2
24
HCO
PaCO
H
Kassirer-Bleich equation
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17. ACID–BASE MONITORING
Acid–base status can be monitored intermittently or
continuously.
Arterial blood gas (ABG) analysis remains the gold
standard in assessing for acid–base disorders.
In the ICU, ABGs can be obtained by arterial
puncture or through an indwelling arterial catheter
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19. SAMPLE ANALYSIS
The blood gas machines in most labs actually
measure the pH ,the pCO2 and the pO2.
bicarbonate level -------- from a serum sample.
The [HCO3-] and the base difference are calculated
values using the Henderson-Hasselbalch equation.
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20. INTERPRETATION OF BLOOD GAS
MEASUREMENTS
It is an easy mathematical exercises
immediately and rapidly get a insight into the underlying
process causing the disturbance in acid–base status.
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21. Acidosis “is a disorder that predisposes/lead to low
systemic pH. Utilizing the Henderson–Hasselbalch
equation, this can be caused by a fall in systemic
bicarbonate concentration or by an elevation in the
pCO2 .
Alkalosis is a disorder that predisposes/lead to high
systemic pH. This is usually caused either by an
increase in systemic bicarbonate concentration or by
a fall in the pCO2. 21
23. FOUR BASIC TYPES OF IMBALANCE
Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis
Respiratory Alkalosis
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24. A change in either the PCO2 or the HCO3 will cause a change
in the pH of extracellular fluid.
When the change involves the PCO2, the condition is called a
respiratory acid-base disorder: an increase in PCO2 is a
respiratory acidosis, and a decrease in PCO2 is a respiratory
alkalosis.
When the change involves the HCO3, the condition is called a
metabolic acid-base disorder: a decrease in HCO3 is a
metabolic acidosis, and an increase in HCO3 is a metabolic
alkalosis.
Acid Base Disorders
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26. ACIDOSIS
Principal effect of acidosis is depression of the CNS
through ↓ in synaptic transmission.
Generalized weakness
Deranged CNS function the greatest threat
Severe acidosis causes
Disorientation
coma
death
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28. ALKALOSIS
Alkalosis causes over excitability of the central
and peripheral nervous systems.
Numbness
Lightheadedness
It can cause :
Nervousness
muscle spasms or tetany
Convulsions
Loss of consciousness
Death
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30. OUTLINE OF ACID-BASE INTERPRETATION
RULES
Step 1 : Determine if data
is consistent using
Henderson’s Equation
Step 2 : Check pH &
PaCO2 (If either of them
is normal, or both are
normal, got to step 6 to
diagnose mixed acid-
base disorder)
Step 3 : Determine
Primary acid base
disorder
Step 4 : Check for
compensation
Step 5 : Check Anion
Gap/hypoalbuminemia or
delta/delta
Step6 : Mix Acid Base
disorders
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32. RESPIRATORY ACIDOSIS
Carbonic acid excess caused by blood levels of
CO2 above 45 mm Hg.
Hypercapnia – high levels of CO2 in blood
Chronic conditions:
Depression of respiratory center in brain that controls
breathing rate – drugs or head trauma
Paralysis of respiratory or chest muscles
Emphysema
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37. RESPIRATORY ALKALOSIS
Carbonic acid deficit
pCO2 less than 35 mm Hg (hypocapnea)
Most common acid-base imbalance
Primary cause is hyperventilation
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38. RESPIRATORY ALKALOSIS
Conditions that stimulate respiratory center:
Oxygen deficiency at high altitudes
Pulmonary disease and Congestive heart failure – caused by
hypoxia
Acute anxiety
Fever, anemia
Early salicylate intoxication
Cirrhosis
Gram-negative sepsis
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42. METABOLIC ACIDOSIS
Bicarbonate deficit - blood concentrations of bicarb drop
below 22mEq/L
Causes:
Loss of bicarbonate through diarrhea or renal dysfunction
Accumulation of acids (lactic acid or ketones)
Failure of kidneys to excrete H+
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43. COMPENSATION FOR
METABOLIC ACIDOSIS
Increased ventilation
Renal excretion of hydrogen ions if possible
K+ exchanges with excess H+ in ECF
( H+ into cells, K+ out of cells)
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46. METABOLIC ALKALOSIS
Bicarbonate excess - concentration in blood is
greater than 26 mEq/L
Causes:
Excess vomiting = loss of stomach acid
Excessive use of alkaline drugs
Certain diuretics
Endocrine disorders
Heavy ingestion of antacids
Severe dehydration
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47. COMPENSATION FOR METABOLIC
ALKALOSIS
Alkalosis most commonly occurs with renal
dysfunction, so can’t count on kidneys
Respiratory compensation difficult – hypoventilation
limited by hypoxia
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49. ANION GAP
This step identifies the type of metabolic acidosis
present, i.e., whether it is secondary to an anion that
creates an AG on electrolyte measurement or not.
The AG is a diagnostic tool to uncover the actual anions
elevated in the blood but not routinely included in our
measurements under normal conditions.
It is calculated as follows:
AG = serum sodium − serum chloride − serum bicarbonate.
A normal anion gap is <12 mmol L−1.
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50. HYPOALBUMINEMIA
In this step interpreting metabolic acidosis is
adjusting for factors that would falsely lower the
anion gap if one existed, e.g.,
hypoalbuminemia and lithium
or bromide ingestion
Adjusted AG in hypoalbuminemia = observed AG +
[2.5(normal albumin − observed albumin)].
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51. DELTA/DELTA
This step is the comparison of the degree of change
in AG with the change in serum bicarbonate, aiming to
assess the extent of contribution of the AG-producing
process to the actual acidosis. This measurement is
called delta/delta:
delta/delta= ΔAG/ ΔHCO- =(AG -12) / (24 - HCO3-).
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52. MNEMONIC VERSION OF EXPECTED COMPENSATORY
RESPONSES TO ACID–BASE DISTURBANCES
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Assuming a normal ABG of pH 7.4, pCO2 40, HCO3− 24,
and utilizing meq L−1 or mmol L−1 for bicarbonate and
mmHg for pCO2,
53. MIXED ACID BASE DISORDER
If the Arterial pH is relatively normal and the PCO2
and/or HCO3 are abnormal, one can assume that a
mixed abnormality is present.
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54. MIXED ACID BASE DISORDER
Diagnosed by combination of clinical assessment, application of
expected compensatory responses , assessment of the anion gap,
and application of principles of physiology.
Respiratory acidosis and alkalosis never coexist
Metabolic disorders can coexist
Eg: lactic acidosis/DKA with vomiting
Metabolic and respiratory AB disorders can coexist
Eg: salicylate poisoning (met.acidosis + resp.alkalosis) 54
55. 1-CASE STUDY
11 year old girl
Mild bronchial asthma with fever and increased
breathing
Asthmaticus diagnosed
ABGs Ph 7.22
p CO2 38mmHg
serum bicarbonate 15med L-1
Serum albumin level 1gdL-1
What is your interpretation …………….?
Hypoalbuminemia ( primary metabolic acidosis and
acute respiratory acidosis )
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56. 2-CASE STUDY
2 year old child was foun unconscious increased
breathing
ABGs pH 7.38
pCO2 28mmHg
serum bicarbonate 16 meqL-1
What is your interpretation……………?
Salicylate poisoning
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