Acid-Base Balance.pptx

Acid-Base Balance and
Disorders
BY
DR. KASIMU SAIDU(M.B.B.S, M.Sc, Ph.D)
SENIOR LECTURER DEPT. OF CHEM PATH & IMM.
Wednesday, March 15, 2023 Dr. K. Saidu (Acid-Balance)

Definition of terms
• pH; is a measure of H+ activity or negative logarithm of hydrogen ion
concentration
• Ka; acid dissociation constant
• pKa; is the negative logarithm of the acid dissociation constant
• Henderson–Hasselbalch equation; An equation that defines the
relationship between pH, bicarbonate, and the partial pressure of
dissolved carbon dioxide gas.

Introduction
• Cells release between 50 and 100 mmol of H+ into the extracellular
fluid (ECF) daily.
• Despite this, the extracellular H+ concentration ([H+]) is maintained at
about 40 nmol/L (pH 7.4).
• To maintain normal/optimal Enzyme activities
• Normal metabolism
• Normal Coordination
• Normal Health
Hydrogen ion balance is largely dependent upon the secretion of H+
from the body into the urine due to renal tubular action.

Introduction
• The tissue cells use the O2 for aerobic
metabolism; some of the carbon in organic
compounds is oxidized to CO2 .
• CO2 diffuses along a concentration gradient
from the cells into the ECF and is returned by
the blood to the lungs, where it is eliminated in
expired air.
Thus the body is dependent upon healthy
function of the kidneys and the lungs for normal
acid–base homeostasis.

Introduction
• The predominant sources of H+ are:
• Anaerobic carbohydrate metabolism produces lactate,
• Anaerobic metabolism of fatty acids by b-hydroxylation
• and of ketogenic amino acids produces acetoacetate, which releases
equimolar amounts of H+. Lactic acidosis or ketoacidosis can occur if
the release of H+ by these reactions exceeds the compensatory
capacity.

Acid-Base
Acid
• Acids can dissociate to produce H+
(protons), which can be accepted by a
base.
• Addition of an acid to a solution,
increases concentration of free H+
in the solution.
• Produces more acidic solution &
decrease in pH

Acid-Base Cont’d
Forms of acid
(a). A strong acid is almost
completely dissociated in
aqueous solution. E.g
hydrochloric acid (Cl– ). HCL
↔ H+ + Cl-
(b). Weak acids dissociate
partially. E.g H2CO3 ↔ HCO3 +
H

Acid-Base
Base
• Bases: A base releases
hydroxyl ions (OH-) in
aqueous solution &
decreases its H+
concentration by accepting or
by binding with free H+.
• This results in increase in pH
of the solution.

Acid-Base
Forms of base
(a) Strong base e.g NaOH
↔Na+ + OH- The OH-, accepts
H+ & results in the formation
of water.
(b) Weak base e.g

Acid-Base
Henderson–Hasselbalch equation
The Henderson–
Hasselbalch equation
expresses the relation
between pH and a
buffer pair – that is, a
weak acid and its
conjugate base

Acid-Base Balance
• Carbon dioxide and H+ are potentially toxic products of aerobic and anaerobic
metabolism respectively.
• Most CO2 is lost through the lungs, but some is converted to HCO3 – , thus contributing
important extracellular buffering capacity;
 The blood pH is maintained in the narrow range of 7.35 - 7.45 (slightly alkaline).
 The body has developed three lines of defense to regulate the body’s acid-base
balance.
 Blood buffers (Chemical)
 Respiratory mechanism (Physiological)
 Renal mechanism (Physiological)

Acid-Base Balance
Buffer
 Blood buffers: A buffer may be defined as a solution of a weak
acid & its salt with a strong base.
 The buffer resists the change in the pH by the addition of acid
or alkali & the buffering capacity is dependent on the absolute
concentration of salt & acid.
 The buffer cannot remove H+ ions from the body but it
temporarily acts as a shock absorbant to reduce free H+ ions.

Acid-Base Balance
Buffer
• Bicarbonate buffer
• Haemoglobin buffer
• Phosphate buffer
• Protein buffer

Acid-Base Balance
Buffer
• Bicarbonate buffer system:
Sodium bicarbonate & carbonic
acid (NaHCO3- H2CO3) is the
most predominant buffer system
of ECF (plasma)

Acid-Base Balance
Buffer
• Hemoglobin binds to H+ ions &
helps to transport CO2 as HCO3 -
with a minimum change in pH.

Acid-Base Balance
Respiratory mechanism
• The rate of respiration, and therefore the rate of CO2 elimination, is
controlled by chemoreceptors in the respiratory centre in the medulla
of the brainstem and by those in the carotid and aortic bodies.
• The receptors respond to changes in the [CO2 ] or [H+] of plasma or
of the cerebrospinal fluid. If the PCO2 rises much above 5.3 kPa, or if
the pH falls, the rate of respiration increases.

Acid-Base Balance
Respiratory control of blood pH is rapid but
only a short term regulatory process, since
hyperventilation cannot proceed for long.

Acid-Base Balance

Acid-Base Balance
Renal mechanism
• Kidney is the only route through which the
H+ can be eliminated from the body. H+
excretion occurs in the proximal
convoluted tubules & is coupled with
• Generation and reabsorption of HCO3-.
Carbonic anhydrase catalyses the
production of carbonic acid (H2CO3) from
CO2 & H2O in renal tubular cells

Acid-Base Disorders

Acid-Base Disorders
Acidosis
• Acidosis occurs if there is a fall in the ratio of [HCO3 – ] to PCO2 in
the ECF. It may be due to:
• Metabolic (non-respiratory) acidosis
• Respiratory acidosis

Acid-Base Disorders
Metabolic acidosis
● Metabolic (non-respiratory) acidosis.
The primary abnormality in the bicarbonate buffer system is a reduction in
[HCO3 – ]
The reduction in the HCO3 – may be due to:
● Its use in buffering H+ more rapidly than it can be generated by normal
homeostatic mechanisms,
● Loss in the urine or gastrointestinal tract more rapidly than it can be
generated by normal homeostatic mechanisms,
● Impaired production.

Metabolic acidosis
Causes
1. Normal anion gap
a. Gastrointestinal causes
i. Diarrhoea
ii. Ureterosigmoidostomy
b. Renal bicarbonate depletion
i. Proximal renal tubular acidosis
ii. Renal insufficiency

Metabolic acidosis
Causes
c. Renal disorder
i. Pyelonephritis
ii. Obstructive uropathy
iii. Distal renal tubular acidosis
d. Ingestion of
i. Ammonium chloride
ii. Excess Intravenous saline

Metabolic acidosis
Causes
2. High anion gap
a. Diabetic ketoacidosis
b. Lactic acidosis
c. Starvation ketoacidosis
d. Alcohol ketoacidosis
e. Salicylate over dose
f. Paraldehyde poisoning
g. Methanol poisoning
h. Ethylene glycol poisoning
i. Renal failure

Metabolic acidosis
Clinical signs and symptoms
a. Tinnitus
b. Oliguria
c. Fruity breath odour
d. Tachypnea or Kussmaul’s breathing
e. Hypotension
f. Shock

Metabolic acidosis
Summary

Concept of plasma anion gap
Anion gap is the difference
between the total
concentration of measured
cations (Na+ and K+) and
measured anions (Cl– and
HCO3 – ); it is normally about
15–20 mEq/L.

Concept of plasma anion gap

Acid-Base Disorders
respiratory acidosis
● Respiratory acidosis, in which the primary
abnormality in the bicarbonate buffer system is
a rise in PCO2 .

Acid-Base Disorders
Respiratory acidosis
Causes
a. Neuromuscular
i. Brain stem injury
ii. High spinal cord injury
iii. Guillain-Barrre syndrome
iv. Myasthenia gravis
v. Botulism
vi. Analgesic, sedative
vii. Pickwickian syndrome
viii. Poliomyelitis
b. Airways obstruction
i. Flail chest
ii. Pneumothorax
iii. Severe pneumonia
iv. Foreign object inhalation
v. Severe pulmonary oedema
vi. Massive pulmonary
embolism
vii. Obstructive pulmonary
disease

a. Headache
b. Dyspnoea
c. Respiratory distress
d. Increased intracranial pressure

Summary

Acid-Base Disorders
Alkalosis
• Alkalosis occurs if there is a rise in the ratio of [HCO3 – ] to PCO2 in
the ECF.
• Metabolic alkalosis
• Respiratory alkalosis

Acid-Base Disorders
Metabolic alkalosis
Metabolic alkalosis the primary abnormality in
the bicarbonate buffer system is a rise in
[HCO3 – ]. There is little compensatory change
in PCO2 .

Metabolic alkalosis
Causes
Chloride responsive (urine chloride ≤20 mmol/L)
• Ingestion of exogenous alkalis, e.g. milk–alkali syndrome (rare) or
salts of strong acids,
• Chloride loss from gastrointestinal tract, e.g. vomiting,
• gastric suction, chloride-losing diarrhoea Chloride loss from skin, e.g.
cystic fibrosis

Metabolic alkalosis
Causes
Chloride unresponsive (urine chloride > 20 mmol/L)
• Severe Hypokalaemia
• Diuretic therapy or exogenous mineralocorticoids, e.g. liquorice
• Severe hypomagnesaemia
• Endogenous mineralocorticoid excess, e.g. Cushing’s syndrome,
• primary hyperaldosteronism (Conn’s syndrome),
• Liddle’s syndrome, 11-hydroxylase and 17-hydroxylase deficiencies,
Bartter’s or Gitelman’s syndrome

Metabolic alkalosis
a. Weakness
b. Muscle cramps
c. Hypoxia
d. Cardiac arrhythmia

Metabolic alkalosis
Summary

Acid-Base Disorders
respiratory alkalosis
Respiratory alkalosis the primary
abnormality is a fall in the PCO2 . The
compensatory change is a fall in [HCO3 – ].

Causes
Central
• Anxiety states
• Head injury,
• cerebral tumour,
• Meningitis
• cerebrovascular accidents
• Salicylates over dose

Causes
Peripheral
• Pulmonary disease, e.g. asthma, pulmonary embolus and pneumonia
• Interstitial lung disease
• High altitude
• Increased cerebral respiratory centre drive, e.g.. pregnancy, heat
exposure, hepatic failure, septicaemia

a. Hyperventilation
b. Paraesthesiae of perioral and extremities
c. Muscle cramps
d. Hyper-reflexia
e. Tachypnea
f. Cardiac arrhythmias
g. Seizures

Acid-Base Disorders
respiratory alkalosis
Summary

Blood gases analysis
Blood gases analyzer

Summary of findings in arterial blood in
disturbances of hydrogen ion homeostasis

Conclusion
• Strict homeostatic control of acid–base balance is essential, otherwise
cell malfunction and death can occur.
• The kidneys excrete non-volatile acid via the renal tubules into the
urine, while the lungs excrete volatile acid as CO2 .
• The major extracellular buffer system involves HCO3 – .
• Blood pH is inversely proportional to the PCO2 and directly proportional
to the [HCO3 – ].

Conclusion
• Respiratory acidosis results from disorders of the respiratory system
and is caused by CO2 retention. Conversely, respiratory alkalosis is
due to excess CO2 loss, as in hyperventilation.
• In the case of the respiratory acidosis, compensation is by the renal
excretion of non-volatile acid and reclamation of HCO3 – .
• In the respiratory alkalosis, the kidneys compensate by losing HCO3 –
.

Conclusion
• Metabolic (non-respiratory) acidosis results from increased non-
volatile acid such as lactic acid or certain ketones.
• Compensation is by the lungs, which increase CO2 excretion by
hyperventilation.
• Metabolic (non-respiratory) alkalosis is caused by HCO3 – excess and
acid loss, such as in prolonged vomiting, and its compensation is via
the lungs, which hypoventilate, thereby retaining volatile acid as CO

THANK YOU

1. The main form in which carbon dioxide is carried from the peripheral
tissue to the lungs is:
• a. Dissolved carbon dioxide
• b. Bicarbonate ion
• c. Carbonate ion
• d. Carbon bound to amino-terminal residues of the globin polypeptide
chain
• e. Complexes with the haeme iron of haemoglobin

2. The main significant kidney defence for respiratory alkalosis
a. High production of K+
b. Reduced secretion of NH3
c. High excretion of HCO3
d. High excretion H+
e. Reduced excretion of Na+

3. Almost 95% of normal healthy subjects have an arterial blood pH
range between;
a. 7.85-7.95
b. 7.25-7.65
c. 6.85-7.05
d. 7.35-7.45
e. 6.15-6.45

4. Metabolic acidosis is associated with;
• a. High blood pH
• b. Low serum or plasma bicarbonate
• c. Hypokalaemia
• d. Relative hypercalcaemia
• e. None of the above

• 5.In repiratory acidosis the blood chemistry is;
• a. Retention of CO2
• b. increased Pco2
• c. increased bicarbonate
• d. Low pH
• e. All of the above

• A 7-year-old boy was admitted unconscious to a casualty department.
On examination he was found to be hyperventilating. He had
inadvertently consumed ethylene glycol antifreeze, which he had
found in his parents’ garage stored in a lemonade bottle. Blood
results were as follows:
• Plasma Sodium 134 mmol/L (135–145) Potassium 6.0 mmol/L (3.5–
5.0) Bicarbonate 10 mmol/L (24–32) Chloride 93 mmol/L (95–105)
Glucose 5.3 mmol/L (3.5–6.0)
• Arterial blood gases pH 7.2 (7.35–7.45) PaCO2 3.18 kPa (4.6–6.0)
PaO2 13.1 kPa (9.3–13.3)

• a. What is the possible diagnosis
• b. What is the reason of low PCO2
• c. Mention 5 other causes of your possible diagnosis

• 1. Write briefly on;
• a. Metabolic acidosis
• b. Metabolic alkalosis
• c. Respiratory acidosis
• d. Respiratory alkalosis
• 2. Write short note on;
• a. Bicarbonate ion
• b. Plasma pH
• c. Henderson-Hasselbalch equation

• 3. What anion gap? Discuss briefly four causes of;
• a. Metabolic acidosis with normal anion gap
• b. Metabolic acidosis with increase or high anion gap

Acid-Base Balance.pptx

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Acid-Base Balance.pptx