Professional Documents
Culture Documents
1
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
2
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-)
3
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
4
Review of acid base homeostasis
5
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
6
Classifying acid-base disorders
7
Case report of respiratory acidosis
9
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)
10
Respiratory acidosis with compensation
mechanisms
↑↑[HCO3-] by kidney
pH = pKa + log
0.03x ↑↑PCO2
Primary
abnormality
14
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
15
Case report on compensated respiratory alkalosis
16
Compensated 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
19
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)
20
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)
21
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)
22
Henderson-Hasselbalch equation in
metabolic acidosis
Primary
abnormality
↓↓[HCO3-]
pH = pKa + log
0.03x ↓↓ PCO2 Compensatory
mechanisms
by lungs
24
Case on metabolic alkalosis
25
Metabolic alkalosis
26
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)
27
Henderson-Hasselbalch equation in
metabolic alkalosis
Primary
abnormality
↑↑[HCO3-]
pH = pKa + log
0.03x ↑↑ PCO2 Compensatory
mechanisms
by lungs
29
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)
30
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
31
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