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ACID – BASE BALANCE
OFONMBUK UMOH
RESIDENT DOCTOR,
DEPT. OF CHEMICAL PATHOLOGY,
UNIVERSITY OF UYO TEACHING HOSPITAL.
OUTLINE
• INTRODUCTION
• DEFINITION OF COMMON TERMS
• HASSELBACH-HENDERSON EQUATION
• ACIDOSIS
• ALKALOSIS
• BLOOD BUFFERS
• SUMMARY
• CONCLUSION
• REFERENCES
INTODUCTION
• ACID –BASE balance is essential for maintenance of body homeostasis
and an imbalance here can lead to several metabolic disturbances.
The role of the buffer systems in the regulation of H+ ions and CO2 is
essential in maintaining a balance.
• The principal
COMMON TERMS
• 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
• Buffer:
 Alkalosis: Physiological state resulting from abnormally high
plasma pH
 Acidosis: Physiological state resulting from abnormally low
plasma pH
 Acidemia: plasma pH < 7.35
 Alkalemia: plasma pH > 7.45
 pH: the negative logarithm to base 10 of the
Hydrogen ion concentration
• Normal body pH →7.35-7.45: All metabolic processes
aim to maintain this pH. Any significant deviation in pH
destabilizes the body’s physiology.
• Buffers: Buffers are usually salts of weak acids (e.g.
NaHC03).
• Buffer Pair: A weak acid and its conjugate base
constitute a buffer pair e.g. H2C03/HC03; NH4
+/NH3;
H2P04
-/HP04
2-
HENDERSON-HASSELBACH EQUATION
This equation was derived by Henderson in 1908 and transformed to its
present form by Hasselbalch in 1916
The action of buffers and their role in maintaining the pH of the system
is aptly captured in the Henderson-Hasselbalch’s equation:
pH = pK + log [Base]
[Acid]
• This equation holds true for all buffer pairs in the body (pk for
H2CO3/HCO3
- = 6.1; H2PO4/HPO4
- = 6.8)
(Conjugate base)
---------------------
(Conjugate acid)
(Conjugate base)
---------------------
(Conjugate acid)
• Because of the logarithmic transformation of the Henderson-
Hasselbatch equation, a pH change of 1 unit denotes a ten-fold
change in [H+].
• pH therefore represents large changes in [H+] in small figures.
Gastrointestinal
Bicarbonate loss
A.Diarrhea
B.Externalpancreaticorsmall-bowel drainage
C.Ureterosigmoidostomy,jejunal loop,ilealloop
D.Drugs
1. Calciumchloride(acidifyingagent)
2. Magnesiumsulfate(diarrhea)
3. Cholestyramine(bileaciddiarrhea)
Renal acidosis
A. Hypokalemia
1. ProximalRTA(type2)
2. Distal(classic)RTA(type1)
B.Hyperkalemia
 LACTICACIDOSIS
 KETOACIDOSIS
 Diabetic
 Alcoholic
 Starvation
 RENALFAILURE (acute and chronic)
Drug-induced hyperkalemia
(with renal insufficiency)
A.Potassium-sparingdiuretics(amiloride, triamterene,
spironolactone)
B.Trimethoprim
C.Pentamidine
D.ACE-IsandARBs
E.Nonsteroidalanti-inflammatory drugs
F.Cyclosporineandtacrolimus
G.Salicylates
 Other
A.Acidloads(ammoniumchloride,
hyperalimentation)
B.Lossofpotentialbicarbonate:ketosis withketone
excretion
C.Expansionacidosis(rapidsaline
administration)
D.Ethylene glycol
E.Methanol
F.Propylene glycol
Causes of Metabolic acidosis
Symptoms of metabolic acidosis are non-specific
and are reflective of the underlying pathology
• Respiratory effects:
 Hyperventilation
 Kausmaul breathing
• CVS:
 ↓ myocardial contractility
 Sympathetic over activity
 Resistant to catecholamines
• CNS:
 Lethargy,disorientation,stupor,muscle
twitching,COMA, CN palsies
• Others : hyperkalemia
Lungs
•Regulate acid-base balance by eliminating or
retaining carbon dioxide
•Does this by altering rate/depth of
respirations
•Faster rate/more depth = get rid of more CO2
and pH rises
•Slower rate/less depth = retain CO2 and pH
lowers
Kidneys
• Regulate by selectively excreting
or conserving bicarbonate and
hydrogen ions
• Slower to respond to change
AcidBaseDisorders
Disorder pH [H+] Primary
disturbance
Secondary
response
   [HCO3
-]  pCO2
   [HCO3
-]  pCO2
   pCO2  [HCO3
-]
   pCO2  [HCO3
-]

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Acid base disturbances

  • 1. ACID – BASE BALANCE OFONMBUK UMOH RESIDENT DOCTOR, DEPT. OF CHEMICAL PATHOLOGY, UNIVERSITY OF UYO TEACHING HOSPITAL.
  • 2. OUTLINE • INTRODUCTION • DEFINITION OF COMMON TERMS • HASSELBACH-HENDERSON EQUATION • ACIDOSIS • ALKALOSIS • BLOOD BUFFERS • SUMMARY • CONCLUSION • REFERENCES
  • 3. INTODUCTION • ACID –BASE balance is essential for maintenance of body homeostasis and an imbalance here can lead to several metabolic disturbances. The role of the buffer systems in the regulation of H+ ions and CO2 is essential in maintaining a balance. • The principal
  • 4. COMMON TERMS • 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 • Buffer:
  • 5.  Alkalosis: Physiological state resulting from abnormally high plasma pH  Acidosis: Physiological state resulting from abnormally low plasma pH  Acidemia: plasma pH < 7.35  Alkalemia: plasma pH > 7.45  pH: the negative logarithm to base 10 of the Hydrogen ion concentration
  • 6. • Normal body pH →7.35-7.45: All metabolic processes aim to maintain this pH. Any significant deviation in pH destabilizes the body’s physiology. • Buffers: Buffers are usually salts of weak acids (e.g. NaHC03). • Buffer Pair: A weak acid and its conjugate base constitute a buffer pair e.g. H2C03/HC03; NH4 +/NH3; H2P04 -/HP04 2-
  • 7. HENDERSON-HASSELBACH EQUATION This equation was derived by Henderson in 1908 and transformed to its present form by Hasselbalch in 1916 The action of buffers and their role in maintaining the pH of the system is aptly captured in the Henderson-Hasselbalch’s equation: pH = pK + log [Base] [Acid] • This equation holds true for all buffer pairs in the body (pk for H2CO3/HCO3 - = 6.1; H2PO4/HPO4 - = 6.8)
  • 8. (Conjugate base) --------------------- (Conjugate acid) (Conjugate base) --------------------- (Conjugate acid)
  • 9. • Because of the logarithmic transformation of the Henderson- Hasselbatch equation, a pH change of 1 unit denotes a ten-fold change in [H+]. • pH therefore represents large changes in [H+] in small figures.
  • 10.
  • 11.
  • 12. Gastrointestinal Bicarbonate loss A.Diarrhea B.Externalpancreaticorsmall-bowel drainage C.Ureterosigmoidostomy,jejunal loop,ilealloop D.Drugs 1. Calciumchloride(acidifyingagent) 2. Magnesiumsulfate(diarrhea) 3. Cholestyramine(bileaciddiarrhea) Renal acidosis A. Hypokalemia 1. ProximalRTA(type2) 2. Distal(classic)RTA(type1) B.Hyperkalemia  LACTICACIDOSIS  KETOACIDOSIS  Diabetic  Alcoholic  Starvation  RENALFAILURE (acute and chronic) Drug-induced hyperkalemia (with renal insufficiency) A.Potassium-sparingdiuretics(amiloride, triamterene, spironolactone) B.Trimethoprim C.Pentamidine D.ACE-IsandARBs E.Nonsteroidalanti-inflammatory drugs F.Cyclosporineandtacrolimus G.Salicylates  Other A.Acidloads(ammoniumchloride, hyperalimentation) B.Lossofpotentialbicarbonate:ketosis withketone excretion C.Expansionacidosis(rapidsaline administration) D.Ethylene glycol E.Methanol F.Propylene glycol Causes of Metabolic acidosis
  • 13. Symptoms of metabolic acidosis are non-specific and are reflective of the underlying pathology • Respiratory effects:  Hyperventilation  Kausmaul breathing • CVS:  ↓ myocardial contractility  Sympathetic over activity  Resistant to catecholamines • CNS:  Lethargy,disorientation,stupor,muscle twitching,COMA, CN palsies • Others : hyperkalemia
  • 14.
  • 15. Lungs •Regulate acid-base balance by eliminating or retaining carbon dioxide •Does this by altering rate/depth of respirations •Faster rate/more depth = get rid of more CO2 and pH rises •Slower rate/less depth = retain CO2 and pH lowers
  • 16.
  • 17.
  • 18. Kidneys • Regulate by selectively excreting or conserving bicarbonate and hydrogen ions • Slower to respond to change
  • 19.
  • 20.
  • 21.
  • 22.
  • 23. AcidBaseDisorders Disorder pH [H+] Primary disturbance Secondary response    [HCO3 -]  pCO2    [HCO3 -]  pCO2    pCO2  [HCO3 -]    pCO2  [HCO3 -]