Patients presenting with hypercarbic respiratory failure are often hypoxic as well. When oxygenation is established, measures should be taken to address the underlying cause of hypercarbia (reversal of drug action, control of fever, or seizures). Patients who are hypercarbic without signs of respiratory fatigue or somnolence may not require intubation based on the Pco2 alone; however, patients with marked increase in the work of breathing or inadequate respiratory effort may require assistance with ventilation.
After identification of the etiology of respiratory failure,specific interventions and treatments are tailored to the needsof the patient. External support of oxygenation and ventilation may be provided by noninvasive ventilation methods (heated humidified high-flow nasal cannula, continuouspositive airway pressure, biphasic positive airway pressure, or negative pressure ventilation) or through invasive methods (traditional mechanical ventilation, high-frequencyoscillatory ventilation, or extracorporeal membrane oxygenation). Elimination of CO2 is achieved through manipulationof minute ventilation (tidal volume and respiratory rate).Oxygenation is improved by altering variables that affectoxygen delivery (fraction of inspired oxygen) or mean airway pressure (PEEP, peak inspiratory pressure, inspiratorytime, gas flow).
The major complication of hypoxic respiratory failure is the development of organ dysfunction. Multiple organ dysfunction includes the development of two or more of the following: respiratory failure, cardiac failure, renal insufficiency/failure, gastrointestinal or hepatic insufficiency, disseminated intravascular coagulation, and hypoxic-ischemic brain injury. Mortality rates increase with increasing numbers of involved organs (see Table 38-3).
Complications associated with mechanical ventilation include pressure-related and volume-related lung injury. Both overdistention and insufficient lung distention (loss of functional residual capacity) are associated with lung injury. Pneumomediastinum and pneumothorax are potential complications of the disease process and overdistention. Inflammatory mediators may play a role in the development of chronic fibrotic lung diseases in ventilated patients.
Prognosis varies with the etiology of respiratory failure. Fewerthan 1% of previously healthy children with bronchiolitis die.Asthma mortality rates, although still low, have increased. Despiteadvances in support and understanding of the pathophysiologyof ARDS, the mortality rate remains approximately 30%.
Prevention strategies are explicit to the etiology of respiratoryfailure. Some infectious causes can be prevented through activeimmunization against organisms causing primary respiratorydisease (pertussis, pneumococcus, Haemophilus influenzae type b) and sepsis (pneumococcus, H. influenzae type b). Passiveimmunization with respiratory syncytial virus immunoglobulins prevents severe illness in highly susceptible patients (prematurity, bronchopulmonary dysplasia). Primary prevention oftraumatic injuries may decrease the incidence of ARDS. Compliance with appropriate therapies for asthma may decrease thenumber of episodes of respiratory failure (see Chapter 78).