- Section 1 ICU organization and management
- Section 2 Pharmacotherapeutics
- Section 3 Resuscitation
- Section 4 The respiratory system
- Part 4.1 Physiology
- Part 4.2 Respiratory monitoring
- Part 4.3 Upper airway obstruction
- Part 4.4 Airway access
- Part 4.5 Acute respiratory failure
- Part 4.6 Ventilatory support
- Part 4.7 Weaning ventilatory support
- Part 4.8 Extracorporeal support
- Part 4.9 Aspiration and inhalation
- Part 4.10 Acute respiratory distress syndrome
- Part 4.11 Airflow limitation
- Part 4.12 Respiratory acidosis and alkalosis
- Chapter 113 Pathophysiology and therapeutic strategy of respiratory acidosis
- Chapter 114 Pathophysiology and therapeutic strategy of respiratory alkalosis
- Part 4.13 Pneumonia
- Part 4.14 Atelectasis and sputum retention
- Part 4.15 Pleural cavity problems
- Part 4.16 Haemoptysis
- Section 5 The cardiovascular system
- Section 6 The gastrointestinal system
- Section 7 Nutrition
- Section 8 The renal system
- Section 9 The neurological system
- Section 10 The metabolic and endocrine systems
- Section 11 The haematological system
- Section 12 The skin and connective tissue
- Section 13 Infection
- Section 14 Inflammation
- Section 15 Poisoning
- Section 16 Trauma
- Section 17 Physical disorders
- Section 18 Pain and sedation
- Section 19 General surgical and obstetric intensive care
- Section 20 Specialized intensive care
- Section 21 Recovery from critical illness
- Section 22 End-of-life care
(p. 521) Respiratory acidosis and alkalosis
Out of 15–30 × 10–3 moles/day of protons derived from the hydration of CO2 only 40–60 × 10–9 moles/day remain unbounded in the plasma. If the CO2 production exceeds the excretion, the CO2 content in plasma and tissue rises (respiratory acidosis) until a new equilibrium is reached. In fact, doubling the PCO2 may compensate the halving of alveolar ventilation with unchanged excretion of the CO2 metabolically produced. Body reacts to respiratory acidosis increasing the secretion of chloride associated with ammonium. The process leads to an increase of bicarbonate in the plasma with an associated increase of pH. All the steps described may be altered in critically-ill patients due to hyper-metabolism, decreased excretion, decreased content of buffering proteins and impaired kidney response. Several options are available for therapy, from mechanical ventilation to artificial lung, up to lung transplant, depending on the severity of clinical conditions and their possible reversibility.
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- Section 1 ICU organization and management
- Section 2 Pharmacotherapeutics
- Section 3 Resuscitation
- Section 4 The respiratory system
- Part 4.1 Physiology
- Part 4.2 Respiratory monitoring
- Part 4.3 Upper airway obstruction
- Part 4.4 Airway access
- Part 4.5 Acute respiratory failure
- Part 4.6 Ventilatory support
- Part 4.7 Weaning ventilatory support
- Part 4.8 Extracorporeal support
- Part 4.9 Aspiration and inhalation
- Part 4.10 Acute respiratory distress syndrome
- Part 4.11 Airflow limitation
- Part 4.12 Respiratory acidosis and alkalosis
- Chapter 113 Pathophysiology and therapeutic strategy of respiratory acidosis
- Chapter 114 Pathophysiology and therapeutic strategy of respiratory alkalosis
- Part 4.13 Pneumonia
- Part 4.14 Atelectasis and sputum retention
- Part 4.15 Pleural cavity problems
- Part 4.16 Haemoptysis
- Section 5 The cardiovascular system
- Section 6 The gastrointestinal system
- Section 7 Nutrition
- Section 8 The renal system
- Section 9 The neurological system
- Section 10 The metabolic and endocrine systems
- Section 11 The haematological system
- Section 12 The skin and connective tissue
- Section 13 Infection
- Section 14 Inflammation
- Section 15 Poisoning
- Section 16 Trauma
- Section 17 Physical disorders
- Section 18 Pain and sedation
- Section 19 General surgical and obstetric intensive care
- Section 20 Specialized intensive care
- Section 21 Recovery from critical illness
- Section 22 End-of-life care