Acid – base disorders

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 Objectives: Acid-base disorders
• Describe the physiological regulation of acid base balance
• Differentiate between metabolic/ respiratory acidosis and
alkalosis
• Describe the causes, compensatory responses and
biochemical basis of treatment of
• metabolic acidosis and alkalosis
• respiratory acidosis and alkalosis
• Identify acid base disorders when arterial blood gas analysis
is provided
• Analyze the compensatory mechanisms that are active in the
four acid base disorders
• Interpret ABG data (pH, PCO2 and HCO3¯ ) and solve
problems related to disorders of acid base balance

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 Review of acid base homeostasis

Bicarbonate buffer
First line of
Chemical
defense against
buffer system Phosphate buffer
pH changes
Protein buffer

Respiratory system
Second line of
Physiological (regulates PCO2)
defense against
mechanisms
pH changes Renal system
(regulates HCO3-)

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 Review of acid base homeostasis
• Buffers are the first line of defense against pH
changes
• Buffers act as immediate acceptors of protons
(H+) generated during metabolism
• The respiratory system responds to pH changes
by altering rates of respiration
– Responds in a few minutes-hours
– When the pH falls (acidosis), there is an increase
in the rate of respiration and increased washout of
CO2
– When the pH increases (alkalosis), there is a
decrease in the rate of respiration and increased
retention of CO2
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 Review of acid base homeostasis

• Renal system responds to pH changes more slowly,

but the response is prolonged
– When the pH falls (acidosis), there is
increased proton secretion in urine and urine
becomes acidic. Phosphate and ammonia
(NH4+) excretion in urine in increased
– When the pH increases (alkalosis), there is
increased HCO3- excretion and urine
becomes alkaline

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 Assessment of acid-base status
• Clinical assessment of acid base status is
done with the help of acid base analyzers
• Acid base parameters assessed by the
clinical laboratory are arterial pH, HCO3-,
and PCO2
• Normal levels
– pH: 7.36-7.44
– PCO2: 38-42 mmHg
– HCO3-: 22-25 mmol/L

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 Classifying acid-base disorders

• Acidosis is a condition in which the pH is less

than 7.36
• Alkalosis is a condition in which the pH is greater
than 7.44
• Respiratory acid base disorders are due to
dysfunction of the respiratory system and are
characterized by primary changes in PCO2
• Metabolic acid base disorders are due to
metabolic or renal disorders and are
characterized by primary changes in the [HCO3-]

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 Case report of respiratory acidosis

Ben, a 45 year old man, has come to the physician.

He has been a chronic smoker for the past 20 years. He
was diagnosed with chronic obstructive pulmonary
disease 2 years ago. Now, he has fever, cough and
dyspnea since yesterday.
The arterial blood gas analysis reveals

– pH: 7.25 Acidosis

– PCO2: 60mmHg (primary disturbance) Respiratory

– [HCO3-]: 26mmol/L
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 Respiratory acidosis
• These disorders are characterized by decreased
rate of respiration/ decreased lung function/
decreased air entry into the lungs
• As a result, the CO2 is NOT washed out,
resulting in elevation of PCO2 (primary
abnormality)
• Remember, CO2 is an ACID, and its
accumulation causes respiratory acidosis
• In the acute stage,
– pH is decreased (lower than 7.36)
– PCO2 is elevated (primary disturbance)
– HCO3- is almost normal

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 Case report on compensated respiratory
acidosis
• Ben, after a few days of onset of the infection (if not
treated).
• Arterial blood gas analysis
– pH: 7.32 (compare to slide 7, pH trying to return to
normal)
– PCO2: 60mmHg (primary change)
– [HCO3-]: 32mmol/L (compensation by the
kidneys)

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Respiratory acidosis with compensation

• During compensation, the renal system comes

to the rescue
• Kidneys excrete more H+, and generate more
HCO3-, and thus the [HCO3-] levels increase
• The excretion of phosphate and ammonia in
urine increase
• In the compensated phase
– pH: pH is lower than normal (<7.36) - closer to normal
pH, when compared to acute stage
– PCO2: Elevated (as the primary defect is still not
corrected – respiratory system is still not functioning
optimally)
– [HCO3-]: Elevated (due to renal compensation)
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 Henderson-Hasselbalch equation in
respiratory acidosis
Compensatory

mechanisms
↑↑[HCO3-] by kidney
pH = pKa + log
0.03x ↑↑PCO2
Primary
abnormality

• Primary abnormality is an ↑↑PCO2 due to

respiratory disease, that results in a fall in pH
• Compensation by the renal system, increases
[HCO3-], and the ratio of [base]/[acid] returns
almost to normal, and pH comes toward normal
(it is still below normal)
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 Causes of respiratory acidosis
Airway
obstruction Central causes:
Opioid drugs,
anesthetics
Disease/injury to the
phrenic nerve; Guillian
Barre syndrome

Chest wall causes:

Lung diseases: muscle diseases
COPD, RDS,
fibrosis of lung

• Drugs that inhibit the respiratory center (opioids)

• Diseases/ injury of the phrenic nerve (supplies diaphragm)
• Lung diseases like chronic obstructive pulmonary disease, fibrosis
of the lung, respiratory distress syndrome in premature infants
• Obstruction to the respiratory tract – due to foreign body in trachea
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 Case report on respiratory alkalosis

• Ann, a 25 year old student has been out camping in

the Himalaya (high altitude). You observe that she is
hyperventilating.
• The second day of her stay, you observe her arterial
blood gas results
• Arterial blood gas results
– pH: 7.50
– PCO2: 20mmHg
– [HCO3-]: 22 mmol/L

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 Respiratory alkalosis
• Respiratory alkalosis is characterized by an increase
in rate of respiration → increased washout of CO2 →
↓↓PCO2 (primary disturbance)
• In the acute stage,
– pH is increased (<7.44)
– PCO2 is ↓↓ (<35mmHg)
– [HCO3-] is almost normal

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Case report on compensated respiratory alkalosis

• You observe Ann after 7 days and repeat

an arterial blood gas analysis
• Arterial blood gas analysis after 7 days
– pH: 7.47 (compared to day 2, it is trying to
return to normal)
– PCO2: 20mmHg (primary disturbance)
– [HCO3-]: 19 mmol/L (renal compensation and
increased HCO3- excretion in urine)

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 Compensated respiratory alkalosis

• During the chronic stage, the renal system tries to bring

the pH back towards normal
• The kidneys do NOT secrete H+ into urine
• There is increased excretion of HCO3- in urine and pH
of urine becomes alkaline, and serum HCO3- falls
• In the compensated phase,
– pH: pH is higher than normal - closer to normal pH, when
compared to acute stage
– PCO2: Decreased (as the primary defect is still not corrected –
respiratory system is still hyperventilating)

– [HCO3-]: Decreased (due to renal compensation)

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 Henderson-Hasselbalch equation in
respiratory alkalosis
Compensatory
mechanisms
↓↓[HCO3-] by kidney
pH = pKa + log
0.03x ↓↓PCO2
Primary
abnormality

• Primary abnormality is an ↓↓ PCO2 due to

hyperventilation, that results in a rise in pH
(alkalosis)
• Compensation by the renal system, decreases
[HCO3-], and the ratio of [base]/[acid] returns
almost to normal, and pH comes toward normal
(it is still above normal)
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 Causes of respiratory alkalosis

• Causes of hyperventilation
– Anxiety, fever, hysteria
– Hypoxia (high altitude) stimulates the respiratory center
and increases the rate of respiration. When a person stays for a
long time at the high altitude, the compensatory mechanisms
are active and [HCO3-] levels fall
– Mechanical ventilation

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 Case on metabolic acidosis
• 26 year old, Dianne (Di) Abeites has been
brought to the ER in an unconscious state. She is
a known type I diabetic on insulin.
• Arterial blood gas analysis on admission
– pH: 7.1
– PCO2: 25mmHg
– [HCO3-]: 15mmol/L (bicarbonate is lost for buffering
ketone bodies – primary abnormality)
• Dipstick test with urine for ketone bodies is
positive
• Di is hyperventilating (Kussmaul breathing)

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 Metabolic acidosis
• Metabolic acidosis is characterized by ↓↓[HCO3-] and low
pH
• [HCO3-] is low either due to increased nonvolatile acids
(HCO3- is lost by buffering) or due to increased losses of
HCO3-
• In the acute stage, (clinically, may not be observed)
– pH is decreased (<7.36)
– PCO2 is almost normal(<40mmHg)
– [HCO3-] is decreased (primary abnormality)

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 Compensated metabolic acidosis
• When the plasma pH falls, the respiratory center is
stimulated, resulting in increased rate of respiration
→ Increased washout of CO2 → ↓↓ PCO2
• If the renal system is functioning, the renal system
can also compensate to increase H+ excretion,
increase the formation of new HCO3-.
• However until the cause of acidosis is treated, pH
does not come back to normal
• In the compensated stage, (clinically more commonly observed)
– pH is lower than normal (<7.36) - closer to normal pH,
when compared to acute stage
– PCO2 is decreased due to compensatory hyperventilation
(<35mmHg)
– [HCO3-] is decreased (primary abnormality)
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 Henderson-Hasselbalch equation in
metabolic acidosis
Primary
abnormality
↓↓[HCO3-]
pH = pKa + log
0.03x ↓↓ PCO2 Compensatory
mechanisms
by lungs

• Primary abnormality is an ↓↓ HCO3- due to loss

of bicarbonate, that results in a fall in pH
• Compensation by the respiratory system, results
in hyperventilation, and decreases PCO2, and
the ratio of [base]/[acid] returns almost to
normal, and pH comes toward normal (it is still
below normal)
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 Causes of metabolic acidosis

Increased production Increased loss of

of non-volatile acids HCO3- (base)

• Diabetic ketoacidosis • Diarrhea (increased

(increased ketone body loss of HCO3- rich
production) intestinal secretions)
• Lactic acidosis • Renal tubular acidosis
(increased lactate (failure to secrete H+
production) and reabsorb HCO3-)
• Chronic renal failure
(decreased excretion of
sulfate, phosphate)

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 Case on metabolic alkalosis

• A 6 month old infant has been brought for

consultation. He had repeated episodes of
vomiting (loss of acid- HCl) for the past
two days.
• Arterial blood gas analysis on admission
– pH: 7.56
– PCO2: 45mmHg
– [HCO3-]: 30mmol/L (primary abnormality)

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 Metabolic alkalosis

• Metabolic alkalosis is characterized by

increased [HCO3-] (relative excess of HCO3-)
• In the acute stage, (clinically, may not be observed)
– pH is increased (greater than 7.44)
– [HCO3-] is increased (greater than 25mmol/L)
(primary abnormality)
– PCO2 is almost normal

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 Compensated metabolic alkalosis
• Increase in the pH (alkalosis) inhibits the respiratory
center, there is a decrease in the rate of respiration
(hypoventilation) → Decreased washout of CO2 (CO2
retention) → ↑PCO2
• Renal system compensates, if it is functioning
normally, by excreting more HCO3- (alkaline urine)
• In the compensated state, (clinically more commonly observed)
– pH is higher than normal (closer to normal pH, when
compared to acute stage)
– [HCO3-] is increased (primary abnormality)
– PCO2 is increased (compensatory mechanism)

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 Henderson-Hasselbalch equation in
metabolic alkalosis
Primary
abnormality
↑↑[HCO3-]
pH = pKa + log
0.03x ↑↑ PCO2 Compensatory
mechanisms
by lungs

• Primary abnormality is an ↑↑HCO3- due to

HCO3- retention, that results in a rise in pH
• Compensation by the respiratory system,
increases PCO2, and the ratio of [base]/[acid]
returns almost to normal, and pH comes toward
normal (it is still above normal)
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 Causes of metabolic alkalosis

• Vomiting, pyloric stenosis resulting in

vomiting
– Loss of acidic contents of the stomach, results
in relative HCO3- excess
• Nasogastric suction
• Excessive consumption of antacids

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 Summary
• First does the patient have an acidosis or
alkalosis
– Look at pH
• Next, what is the primary problem? Is it
metabolic or respiratory?
– Look at PCO2 and pH,
• If the PCO2 change is the opposite direction of the
pH change, then it is a respiratory disorder
– Eg: If pH- low and PCO2- high (respiratory)
• If the PCO2 change is in the same direction as pH
change, then it is a metabolic disorder
– Eg: If pH-low and PCO2- low (metabolic)

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 Summary
pH PCO2 - Causes of the
HCO3 disturbance
Normal
Acute
Respiratory
acidosis Compensated

Uncompensated
Respiratory
alkalosis Compensated

Uncompensated
Metabolic
acidosis Compensated

Uncompensated
Metabolic
alkalosis Compensated

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 The acid base data of a patient are:
pH=7.22; PCO2 =20mm Hg; HCO3-=15mEq/L.
(Normal: pH=7.4; PCO2 =40mm Hg; HCO3-=24mEq/L).
He is in a state of

1. Uncompensated metabolic acidosis

2. Uncompensated metabolic alkalosis
3. Compensated metabolic acidosis
4. Compensated respiratory acidosis
5. Uncompensated respiratory alkalosis
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