Acid Base Balance

ANUSHA GANGADHARAN
GROUP 8
A BIT TO THE BASICS .........
 An acid is a substance that releases (“donates”) a
hydrogen ion (H+ ). An acid (HA) can dissociate into a
hydrogen ion (H+) and a conjugate base (A− )
 A base is a substance that accepts a hydrogen ion.
 pH is the negative log of hydrogen ion concentration.
 pH = -log[H+]
 pKa determines the strength of the acid. It is pH at which
50% of acid is dissociated into its conjugate base

OUR BODY AND PH
 Homeostasis of pH is tightly controlled
 pH of Extracellular fluid = 7.4
 pH of Blood = 7.35 – 7.45
 pH < 6.8 or > 8.0 death occurs
 Acidemia below 7.35
 Alkalemia above 7.45

WHY IS ACID-BASE BALANCE IMPORTANT ?
 Acid-base balance can also affect electrolytes (Na+, K
+
,Cl-)
 Affects membrane functions, alter protein functions, etc.
 Can also affect hormones
 Small changes in pH can produce major disturbances
 Two types of acids are produced in the body:

 Volatile acids : Carbonic acid formed from CO2
 Non-volatile acids: incomplete metabolism of protein,

lipids e.g. lactic acid, keto acid, sulphuric acids
REGULATION OF BLOOD PH
 To maintain the blood pH at 7.35 –7.45, there are three
primary systems that regulate the hydrogen ion
concentration in the body fluids.
 These are :
HENDERSON HASSELBALCH EQUATION
 The Henderson-Hasselbalch equation expresses the
relationship among pH, pKa , and the concentrations of
an acid and its conjugate base.
BUFFER SYSTEM
 These are the first line of defence against pH change
 React very rapidly within seconds.
 The buffer systems of the blood, tissue fluids and cells;

immediately combine with acid or base to prevent
excessive changes in pH.
 It do not eliminate hydrogen ions from the body or add
them to the body but only keep them tied up until balance
can be re-established.
 Three major chemical buffer systems
1. Bicarbonate buffer
2. Phosphate buffer
3. Protein buffer
BICARBONATE BUFFER SYSTEM
 Bicarbonate buffer is the most important extracellular fluid
buffer.
 Bicarbonate buffer constitute sodium bicarbonate
(NaHCO3-) and carbonic acid (H2CO3).
 Carbonic acid dissociates into hydrogen and bicarbonate
ions.
 Under normal circumstances there is much more
bicarbonate present than carbonic acid (the ratio is
approximately 20:1).
ALKALI RESERVE
 Plasma Bicarbonate (HCO3-) represents the alkali reserve
and it has to be sufficiently high to meet the acid load.
 If it was too low to give a ratio of 1, all the HCO3-
would have been exhausted within a very short time; and

buffering will not be effective.
 So, under physiological circumstances, the ratio of 20:1
(a high alkali reserve) ensures high buffering efficiency
against acids.
PHOSPHATE BUFFER SYSTEM
 It is not important blood buffer.
 It plays a major role in buffering renal tubular fluid and
the intracellular fluid.
 The normal ratio of Na2HPO4 and NaH2PO4 in plasma is
4:1 and this is kept constant by the help of kidneys for

which phosphate buffer system is directly related to the
kidneys
PROTEIN BUFFER SYSTEM
 In the blood, plasma proteins especially albumin act as
buffer because:
 It contain a large number of dissociable acidic (COOH)
and basic (NH2) groups.

 In acid solution, NH2 accept excess H+
 In basic solutions, COOH give up H+
 Other important buffer groups of proteins in the
physiological pH range, are the imidazole groups of
histidine.
HEMOGLOBIN BUFFER SYSTEM
 Hemoglobin buffers in RBC plays an important role in
respiratory regulation of pH.
 It helps in transport of metabolically produced CO2 from
cell to lungs for excretion.

 As hemoglobin releases O2 it gains a great affinity for
H+
RESPIRATORY BUFFER
 Respiratory mechanism is called second line of defence.
 It is achieved by regulating the concentration of
carbonic acid (H2CO3) in the blood and other body fluids
by the lungs.
 The respiratory center regulates the removal or retention
of CO2 and thereby H2CO3 from the extracellular fluid by
the lungs.
 Thus lungs, function by maintaining one component
(H2CO3) of the bicarbonate buffer
RENAL BUFFERING
 The role of kidneys in the maintenance of acid base
balance of the body is highly significant.
 The renal mechanism tries to provide a permanent
solution to the acid-base disturbances.
 This is in contrast to the temporary buffering system and
a short term respiratory mechanism.
 The kidneys regulate the blood pH by maintaining the
alkali reserve.
RENAL MECHANISM
 The renal mechanism of acid base balance is achieved
by:
 Excretion of H+ ions
 Reabsorption of bicarbonate
 Excretion of titratable acid
 Excretion of ammonium ions.

ACIDIFICATION OF URINE
 The pH of urine is normally acidic (6.0).
 This clearly indicates that the kidneys have contributed
to the acidification of urine, when it is formed from the
blood plasma (pH 7.4).
 In other words, the H+ ions generated in the body in the
normal circumstances are eliminated by acidified urine.
 Hence the pH of urine is normally acidic (6.0), while that
of blood is alkaline (7.4).
 Urine pH, however, is variable and may range between
4.5-9.5, depending on the concentration of H+ ions.
ACID-BASE IMBALANCES
 pH< 7.35 acidemia
 pH > 7.45 alkalemia
 The body response to acid-base imbalance is called

compensation
 May be complete if brought back within normal limits
 Partial compensation if range is still outside norms.

STEPS TO THE CLINICAL ASSESSMENT
OF ACID-BASE DISTURBANCES
1. Assess pH (normal 7.4); pH <7.38 is acidemia and >7.42
is alkalemia
2. Serum bicarbonate level (normal : 24)
3. Assess arterial pCO2 (normal 40)
4. Check compensatory response
5. Assess anion gap.
6. Assess the change in serum anion gap/change in
bicarbonate.
7. Assess if there is any underlying cause.
APPROPRIATE COMPENSATION
ANION GAP
 The anion gap is a biochemical tool which sometimes
helps in assessing acid-base problems.
 It is used for the diagnosis of different causes of
metabolic acidosis.
 Anion gap is defined as the difference between the total
concentration of measured cations (Na+ and K+) and that
of measured anion (Cl- and HCO3-).
METABOLIC ACIDOSIS
 Metabolic acidosis can be defined as primary decrease in
[HCO3]
1. Consumption of HCO3 by a strong non-volatile acid
2. Renal or gastrointestinal wasting of bicarbonate
3. Rapid dilution of ECF compartment with a
bicarbonate free fluid.
ETIOLOGY
INCREASED ANION GAP
Lactic Acidosis
 Tissue hypoxia
 Shock
 Hypoxemia
 Severe anemia
 Liver failure
 Malignancy
 Intestinal bacterial overgrowth
 Inborn errors of metabolism
 Medications
 Nucleoside reverse transcriptase inhibitors
 Metformin
 Propofol
Ketoacidosis
 Diabetic ketoacidosis
 Starvation ketoacidosis
 Alcoholic ketoacidosis
Kidney Failure
Poisoning
 Ethylene glycol
 Methanol
 Salicylate
 Toluene
 Paraldehyde
Normal Anion Gap (HYPERCHLOREMIC)
 Diarrhea
 Renal tubular acidosis (RTA)
 Distal (type I) RTA
 Proximal (type II) RTA
 Mixed (type III) RTA
 Hyperkalemic (type IV) RTA
 Urinary tract diversions
 Posthypocapnia
 Ammonium chloride intake

PATHOGENESIS
 1. Loss of bicarbonate from the body
 2. Impaired ability to excrete acid by the kidney
 3. Addition of acid to the body (exogenous or

endogenous)
CLINICAL FEATURES
 CARDIOVASCULAR
1. Impairment of cardiac contractility
2. Arteriolar dilatation, venoconstriction, and
centralization of blood volume
3. Increased pulmonary vascular resistance
4. Reduction in cardiac output, arterial blood pressure,
and hepatic and renal blood flow
5. Sensitization to re-entrant arrhythmias and reduction in
threshold of ventricular fibrillation
6. Attenuation of cardiovascular responsiveness to
catecholamines
RESPIRATORY
 Hyperventilation-Kussmaul breathing is the very deep and labored
breathing
 Decreased strength of respiratory muscles and promotion of
muscle fatigue
 METABOLIC
Increased metabolic demands
Insulin resistance
Inhibition of anaerobic glycolysis
Reduction in ATP synthesis
Hyperkalemia
Increased protein degradation
CNS
 Inhibition of metabolism and cell-volume regulation
 Headache
 Lethargy
 Confusion
 Coma
TREATMENT
GENERAL MEASURES
 Any respiratory component of acidemia should be
corrected.
 If arterial pH remains below 7.20; alkali therapy usually
in the form of NaHCO3(usually a 7.5% solution) may be
necessary.
 Half of the calculated deficit should be administered
within the first 3–4 hours to avoid overcorrection.
 Large amounts of HCO 3- may have deleterious effects
SPECIFIC THERAPY
 DIABETIC KETOACIDOSIS:
1. Replacement of existing fluid deficit
2. Insulin
3. Potassium, phosphate and magnesium
 ALCOHOLIC KETOACIDOSIS,
Thiamine
 SALICYLATE-INDUCED ACIDOSIS:
1. Vigorous gastric lavage with isotonic saline (not NaHCO3)
2. Alkalinization of urine with NaHCO3 to a pH >7.5 increases

elimination of salicylate.
 ETHYLENE GLYCOL—INDUCED ACIDOSIS:
1. Saline or osmotic diuresis

2. Ethanol
3. Hemodialysis
METABOLIC ALKALOSIS
 Manifested by an elevated arterial pH
 Increase in the serum [HCO3-]
 Increase in PaCO2 as a result of compensatory alveolar

hypoventilation.
 It is often accompanied by hypochloremia and
hypokalemia
PATHOGENESIS
 Metabolic alkalosis occurs as a result of net gain of
[HCO3-] or loss of non-volatile acid (usually HCl by
vomiting) from the extracellular fluid.
 Metabolic alkalosis represents a failure of the kidneys to
eliminate HCO3 - in the usual manner.
 The kidneys will retain, rather than excrete, the excess
alkali and maintain the alkalosis if
1. Volume deficiency, chloride deficiency, and K+
deficiency exist in combination with a reduced GFR,
which augments distal tubule H+ secretion.
2. Hypokalemia exists because of autonomous
hyperaldosteronism.
PHYSIOLOGIC EFFECT OF ALKALOSIS
 Alkalosis increases affinity of Hb for O2 and shifts the
ODC to the left, making it more difficult for Hb to give
up O2 to tissues.
 Movement of H+ out of the cells in exchange of
extracellar K+ into cells, can produce hypokalaemia.
 Alkalosis increases the number of anionic binding sites
for Ca2+ on plasma proteins and can therefore decrease
ionized plasma [Ca2+] leading to circulatory depression
and neuromuscular irritability.
SYMPTOMS
TREATMENT
 Primary treatment is correcting the underlying stimulus
for HCO3 - generation.
 Proton pump inhibitors or the discontinuation of
diuretics.
 Isotonic saline
 Acetazolamide
 Dilute hydrochloric acid (0.1 N HCl)
 Hemodialysis against a dialysate low in [HCO3- ] and

high in [Cl-]
1.Mr. X is admitted with severe attack of asthma. Her
arterial blood gas result is as follows:
 pH : 7.22
 PCO2 : 55
 HCO3- : 25
A. Respiratory Acidosis
B. Respiratory .Alkalosis
C. Metabolic. Acidosis
D. Metabolic. Alkalosis
2.Mr. D is admitted with recurring bowel obstruction has
been experiencing intractable vomiting for the last
several hours. His ABG is:
 pH : 7.5
 PaCO2 :42
 HCO3- : 33
A. Respiratory Acidosis
B. Respiratory Alkalosis
C. Metabolic Acidosis
D. Metabolic Alkalosis
3.The pH of the body fluids is stabilized by buffer systems.
Which of the following compounds is the most effective
buffer system at physiological pH ?
1. Bicarbonate buffer
2. Phosphate buffer
3. Protein buffer
4. Bone buffer
5. All of the above

4. A person was admitted in a coma. Analysis of the arterial
blood gave the following values:
pH 7.1
PCO2 16 mm Hg
HCO 3- 5 mEq/L and
What is the underlying acid-base disorder?

 Metabolic Acidosis
 Metabolic Alkalosis
 Respiratory Acidosis
 Respiratory Alkalosis
5. All are true for renal handling of acids in metabolic
acidosis except
1. Hydrogen ion secretion is increased
2. Bicarbonate reabsorption is decreased
3. Urinary acidity is increased
4. Urinary ammonia is increased
5. Bicarbonate reabsorption is increased

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ANUSHA GANGADHARAN

 pH is the negative log of hydrogen ion concentration.

 pKa determines the strength of the acid. It is pH at which

50% of acid is dissociated into its conjugate base

 pH of Blood = 7.35 – 7.45

 pH < 6.8 or > 8.0 death occurs

 Acidemia below 7.35

 Alkalemia above 7.45

 Can also affect hormones

 Small changes in pH can produce major disturbances

 Two types of acids are produced in the body:

 Non-volatile acids: incomplete metabolism of protein,

 The buffer systems of the blood, tissue fluids and cells;

would have been exhausted within a very short time; and

4:1 and this is kept constant by the help of kidneys for

and basic (NH2) groups.

cell to lungs for excretion.

 Excretion of titratable acid

 Excretion of ammonium ions.

 The body response to acid-base imbalance is called

 Partial compensation if range is still outside norms.

 Intestinal bacterial overgrowth

 Inborn errors of metabolism

 Nucleoside reverse transcriptase inhibitors

 Renal tubular acidosis (RTA)

 Distal (type I) RTA

 Proximal (type II) RTA

 Mixed (type III) RTA

 Hyperkalemic (type IV) RTA

 Urinary tract diversions

 Ammonium chloride intake

 3. Addition of acid to the body (exogenous or

1. Vigorous gastric lavage with isotonic saline (not NaHCO3)

2. Alkalinization of urine with NaHCO3 to a pH >7.5 increases

1. Saline or osmotic diuresis

 Increase in PaCO2 as a result of compensatory alveolar

 Dilute hydrochloric acid (0.1 N HCl)

 Hemodialysis against a dialysate low in [HCO3- ] and

5. All of the above

What is the underlying acid-base disorder?

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