The acid base “balance”
Abelow, Understanding Acid-Base, Williams & Wilkins 1998
(Abelow B, 1998 “Understanding Acid-Base”)
(Abelow B, 1998 “Understanding Acid-Base”)
Neuromuscular chain defects
-may alter alveolar ventilation
(Abelow B, 1998 “Understanding Acid-Base”)
Pulmonary diseases
-may alter alveolar ventilation
(Abelow B, 1998 “Understanding Acid-Base”)
HENDERSON-HASSELBALCH EQUATION
pH = pK + log [HCO3-]/0.03PCO2
pH = 6.1 + log 24/(0.03 x 40)
pH = 6.1 + log 24/1.2
pH = 6.1 + log 20
pH = 6.1 + 1.3
pH = 7.4
(Abelow B, 1998 “Understanding Acid-Base”)
Renal bicarbonate reabsorption
Abelow, Understanding Acid-Base, Williams & Wilkins 1998
Distal nephron luminal H+/K+ exchanger
(Abelow B, 1998 “Understanding Acid-Base”)
Abelow, Understanding Acid-Base, Williams & Wilkins 1998
RESPIRATORY ACIDOSIS
:
:
Alveolar hypoventilation
acute airway obstruction with underventilation
Late acute asthma, acute COPD
CNS
- opiate overdose
- stroke
- neuropathy, myopathy
COMPENSATED RESPIRATORY ACIDOSIS
UNCOMPENSATED RESPIRATORY ACIDOSIS
Abelow, Understanding Acid-Base, Williams & Wilkins 1998
RESPIRATORY ALKALOSIS
- Alveolar hyperventilation
: Early acute asthma with over ventilation
: Pulmonary embolus, pneumonia, pulmonary
oedema
: Anxiety
RESPIRATORY ALKALOSIS
Uncompensated
Compensated
Abelow, Understanding Acid-Base, Williams & Wilkins 1998
METABOLIC ACIDOSIS
- xs production of H+ ions
: Diabetic ketoacidosis
: Acute renal failure
: Circulatory shock (eg septic, cardiogenic,
hypovolemic)
METABOLIC ACIDOSIS WITH RESPIRATORY
COMPENSATION
UNCOMPENSATED METABOLIC ACIDOSIS
Abelow, Understanding Acid-Base, Williams & Wilkins 1998
METABLOIC ALKALOSIS
- xs HCO3- ions
: Loss of gastric fluid – vomiting
: Diuretics-K+ loss: xs renal HCO3reabsorption
:Post hypercapnic mechanical ventilation
METABOLIC ALKALOSIS
Abelow, Understanding Acid-Base, Williams & Wilkins 1998
When you see “respiratory”, think PCO2
and
When you see “metabolic”, think [HCO3-]
Abelow, Understanding Acid-Base, Williams & Wilkins 1998
Name
Change
Description
Respiratory acidosis
 PCO2
Hypercapnic acidosis
Respiratory alkalosis
 PCO2
Hypocapnic alkalosis
Metabolic acidosis
 [HCO3-]
Hypobicarbonatemic acidosis
Metabolic alkalosis
 [HCO3-]
Hyperbicarbonatemic alkalosis
Abelow, Understanding Acid-Base, Williams & Wilkins 1998
EVALUATION OF BLOOD GASES
Abelow, Understanding Acid-Base, Williams & Wilkins 1998
Abelow, Understanding Acid-Base, Williams & Wilkins 1998
RESPIRATORY FAILURE
Type 1:
PaO2 PaCO2
- Alveolar hyperventilation
Type 2:
PaO2 PaCO2
- Alveolar hypoventilation
ACUTE ASTHMA
Early:
Alveolar hyperventilation
-  respiratory drive
PaO2 PaCO2
 give high concentration of O2 (60%)
Late:
Alveolar
hypoventilation
- respiratorydrive
PaO2 PaCO2
: still relying on hypercapnic drive
 give high concentration of O2 (60%)
- may need mechanical ventilation
ACUTE EXACERBATION OF COAD
•
Chronic alveolar hypoventilation
-  respiratory drive
- switch from hypercapnic to hypoxic drive

Use low concentration of O2 (24%) to avoid
suppressing hypoxic drive

Can use central respiratory stimulation
(doxapram) to permit higher concentration O2
(28-35%)
ARTERIAL BLOOD GASES IN ACUTE ASTHMA
Late Stage = Fatigue = Alveolar hypoventilation
Early Stage = Alveolar hyperventilation
PaO2
1KPa = 7.5 mm Hg
PaCO2
If high PaCO2 (> 6KPa) and low PaO2 (< 8KPa) at presentation, or if rising PaCO2 and
falling PaO2 despite treatment  mechanical ventilation (ie call anaesthetist)
Always use high flow O2 mask (> 60% inspired concentration) in acute asthma - even if high
PaCO2 - as patient still relying on hypercapnic drive