Abelow, Understanding Acid-Base, Williams & Wilkins 1998

The acid base “balance” Abelow, Understanding Acid-Base, Williams & Wilkins 1998

(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

EVALUATION OF BLOOD GASES 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

Abelow, Understanding Acid-Base, Williams & Wilkins 1998